# Question
Title: Why is labeling a cognitive distortion? How is it different from categorization?
Is there any difference between label and category? We use categories everyday. Psychiatrists use it too. Aren't psychiatric disorders like schizophrenia or bipolar disorder just labels that are assigned to specific disorder cases that patients have?

Isn't "labeling" itself a label? People have some thoughts, but some of them are labeled as "labeling".

If I say that the bird I see is a pigeon, this is labeling as well. But I don't think that saying that the pigeon is a pigeon is a cognitive distortion.

Sorry, I am not a psychologist. But my psychotherapist said me that I assign labels to person and their actions. But I don't understand what it means and why it is bad.

# Answer
> 2 votes
#### Scientific labeling:

* If you study arthropods long enough, you will find that many of them have two pairs of antennae. We call these creatures **crustaceans**.

#### Cognitively distorted labeling:

* If you study arthropods long enough, you will find that many of them lack coherent goals in life and generally fail to accomplish anything meaningful. We call these creatures **losers**.

Science, as a discipline, uses labeling just as you mention. Biologists label creatures to fit them into categories based on their ancestry and features. Psychologists classify mental health conditions into diagnoses such as depression and schizophrenia to aid research and treatment. Astronomers divide heavenly bodies into classifications such as stars, planets, dwarf planets, moons, comets, and asteroids.

Scientists sometimes disagree on the best classification system, the exact set of labels to use, or exactly what should get each label. In 2006, the International Astronomical Union (IAU) created the new label of dwarf planet and reclassified several worlds into this new category, including the formerly classified as planet Pluto and the formerly classified as asteroid Ceres. The fact that there has been a relabeling or that there is a disagreement does not mean that cognitive distortions are being used if the labeling systems being used are founded on logically and empirically reasonable models.

#### Learning about idiots, losers, has-beens, never-wases, stupid people, and uglies.

Labeling, as a cognitive distortion, is not simply attaching a label to something. It is a pathological process of attaching an extreme and ambiguous label to something in a manner not warranted by the evidence. Read resources on labeling as a distortion. Nearly all of them give examples such as "loser", "failure", "bad", or "pathetic". Note a trend here. These are statements of opinion, not fact, and they are applied in such a way as to be *unfair* to the target.

Now, let's consider a scenario. You're a gay Scottish dentist. You have several labels but they are all completely factual and value-neutral. You go to your local singles mixer and identify yourself as such, and maybe even add a nice opinion label like "cute" or "cool" to yourself. There is no distortion here.

Now, you botch a root canal and are in the depths of despair. You call your sister frantically and call yourself a "loser" and a "failure" who should "never be allowed to practice dentistry ever again". Now we are getting into cognitive distortion territory. Maybe you made a mistake. Maybe you were even reckless. These things don't define *who you are as a person*. Cognitive distortions are acts of unfair or unreasonable mislabeling that accomplish no good but instead cause psychological distress. Calling a duck a duck is not distortion, but good science.

Ways to approach this:

* You are a person who made a mistake. You are not a mistake.
* You are a person who screwed up. You are not a screw-up.
* You may have failed this time. You are not a failure.

# Answer
> 2 votes
As Bryan Krause suggested (above), talking with your psychotherapist is likely the **most important** next step for you to take.

Also, please note that what I write below is simply general *information* about cognitive behavioral therapy. I do not know your situation. What I share with you here is not personal advice. It is information only.

You might find it helpful to read more about cognitive behavioral therapy (CBT) because it might answer at least one of your questions, which I will paraphrase as: *Why are cognitive distortions potentially harmful?*

### Brief answer with an example

What you *think* (assumptions, beliefs) about yourself and the world greatly influences what you *do* (behavior) and how you *feel* (emotions). Our minds often distort reality by "telling" us untruths, which in turn lead us to feel and act differently.

Example: I'm a college student majoring in psychology. I studied reasonably well for a statistics test, but I received a "B-" grade. My friend received an "A". I immediately think, "I'm not smart enough to be a psychologist." I subsequently don't study as hard and I start thinking about changing to an "easy" major. I feel down and start to smoke weed every day to feel better, which causes me to feel even less motivated.

Thus, according to cognitive behavioral theory, my negative (distorted) thoughts about the "B-" grade led to a downward spiral of maladaptive behaviors and depressed mood.

### Very brief history

\[**Edit of 17 Dec 2020**: Thank you to tale852150 for calling attention to my egregious and baffling omission (see the Comments, below). I added this section about Albert Ellis because Ellis was indeed the first cognitive-behavioral theorist and clinician.\]

**Albert Ellis (1913–2007)**

In the mid-1950s, Albert E. Ellis, Ph.D., developed the first systematic cognitive therapy, which he originally called "rational therapy", with the therapy approach evolving, the name changed to "rational-emotive therapy" (RET), and finally, "rational-emotive behavior therapy" (REBT). This book chapter provides a concise, yet complete overview of REBT:

Dryden, Windy, Daniel David, and Albert Ellis. "Rational Emotive Behavior Therapy." In *Handbook of Cognitive Behavioral Therapies*, 3rd ed., edited by Keith S. Dobson, 226–276. New York: Guilford, 2010.

And here are few representative samples of Ellis' publications:

Ellis, Albert. "Rational Psychotherapy and Individual Psychology." *Journal of Individual Psychology* 13, no. 1 (1957): 38-44.

Ellis, Albert, and Robert A. Harper. *A New Guide to Rational Living*. Englewood Cliffs, NJ: Prentice-Hall, 1961.

Ellis, A. (1962). *Reason and Emotion in Psychotherapy*. Secaucus, NJ: Lyle Stuart.

Ellis, Albert. "Rational-Emotive Therapy and Cognitive Behavior Therapy: Similarities and Differences." *Cognitive Therapy and Research* 4, no. 4 (1980): 325-340.

Ellis, Albert. "Changing Rational-Emotive Therapy (RET) to Rational Emotive Behavior Therapy (REBT)." *Journal of Rational-Emotive and Cognitive-Behavior Therapy* 13, no. 2 (1995): 85-89.

**Aaron Beck (1921– )**

Aaron Beck, M.D. developed "cognitive therapy" in the early 1960s. One of his first breakthrough articles was:

Beck, Aaron T. "Thinking and Depression: I. Idiosyncratic Content and Cognitive Distortions." *Archives of General Psychiatry* 9, No. 4 (1963): 324–333. doi:10.1001/archpsyc.1963.01720160014002

### Helpful articles

John M. Grohol, "15 Common Cognitive Distortions", *PsychCentral* (24 Jun 2019). Here is a quote from Dr. Grohol's article:

> What’s a *cognitive distortion* and why do so many people have them? Cognitive distortions are simply ways that our mind convinces us of something that isn’t really true. These inaccurate thoughts are usually used to reinforce negative thinking or emotions — telling ourselves things that sound rational and accurate, but really only serve to keep us feeling bad about ourselves.

Cherry, Kendra. "What Is Cognitive Behavioral Therapy (CBT)?" *verywellmind* (13 June 2020). This is a quote from the article:

> Cognitive behavioral therapy focuses on changing the automatic negative thoughts that can contribute to and worsen emotional difficulties, depression, and anxiety. These spontaneous negative thoughts have a detrimental influence on mood.

Note that "automatic negative thoughts" and "cognitive distortions", as used by most psychotherapists, have very similar if not identical meanings.

### Best-selling book

The top-selling cognitive behavioral therapy book on Amazon.com currently is:

Gillihan, Seth J. *Cognitive Behavioral Therapy Made Simple: 10 Strategies for Managing Anxiety, Depression, Anger, Panic, and Worry*. Emeryville, CA: Althea Press (Callisto Media), 2018. (Amazon rating/reviews: 4.6 stars; ReviewMeta: 4.6 stars)

I haven't read Gillihan's book, but a ReviewMeta rating of 4.6 based on 97 reviews suggests it's been helpful to most people.

Of course, there are scores of good online articles and books about cognitive behavioral therapy. The ones I mentioned are just a select sample to (hopefully) get you started learning more.

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Tags: cognitive-psychology, cbt, cognitive-distortion
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# Question
Title: How did the very rapid nature of Russian industrialisation/collectivisation affect peoples capacity for abstract thinking?
I am sure I read once about research conducted on villagers who were pushed very very quickly from very basic, premodern agrarian structures into collectivised, quota-driven, management-structure based farming and the effects this had on their thinking and cognition.

It is one of those periods that seems artificial and extreme and thus ripe for interesting research, but every time I Google to try and track down the original source I can't find it under the deluge of papers exploring the economics or changes to social environments. I can't quite find the right keywords...

Can anyone who sees this remember any research into changes in the way people thought, within the same generation, that biased them into thinking more about abstract groups and categories and mathematical concepts rather than more basic immediate thought patterns? This may or may not have used IQ to measure capacity for abstract thought but I am not sure.

Any help would be greatly appreciated! It must have been an interesting time to study all sorts of questions, and the time scale required for these shifts in thought patterns would be interesting

# Answer
> 2 votes
You are probably thinking of Alexander Luria's "On the historical development of cognitive processes" (1974). Luria was a Soviet psychologist who studied rural people in the Soviet Union and observed their apparent lack of ability to move from concrete to abstract thought.

See the TED talk "Why our IQ levels are higher than our grandparents'" by James Flynn, the discoverer of the so-called Flynn effect in educational psychology, where he specifically mentions Luria's rural research and how 20th century progress brought abstract reasoning into the necessary toolbox of a larger and larger proportion of populations.

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Tags: social-psychology, intelligence
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# Question
Title: Term for how anxiety makes people think abnormally?
For a paper I'm writing, I want to make a point about how anxiety changes the way people think - i.e., the same person in the same situation might think differently depending on whether or not they are anxious.

The problem is that I'm not sure what search term to use to find papers that may be relevant, so I was just wondering if anyone else knows.

# Answer
A general term is cognitive distortion:

> ... an exaggerated or irrational thought pattern involved in the onset or perpetuation of psychopathological states, such as depression and anxiety.

Not sure if there are more emotion-specific terms.
> 3 votes

# Answer
I think 'cognitive distortion' is a good one, like @Arnon Weinberg mentioned.

You will probably also find some useful papers with ''anxiety''+''cognitive bias''. E.g. this paper

> The existence of cognitive biases in anxiety is now well established, and we summarize evidence demonstrating attentional vigilance to cues associated with threat, pessimistic interpretation of ambiguous items and an increased perception of the likelihood of occurrence of negative events.

Bias you can further split up in ''attentional bias'' or ''memory bias''.
> 2 votes

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Tags: emotion, terminology, abnormal-psychology, clinical-psychology, anxiety
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# Question
Title: How does acute tryptophan depletion work?
The literature online about this practice is very poor. The theory goes like this:

* A mix of amino acids that does not include tryptophan will lower the proportion of tryptophan in the bloodstream.
* Transporter molecules will have a harder time finding free tryptophan and thus not bring it back to the brain for synthesis into serotonin.
* Serotonergic neurotransmission will drop acutely.

That last part is what does not make sense to me. Even if insufficient tryptophan is coming into the brain, don't the neurons already have plenty of serotonin stored in the axon vesicles from which the neurotransmission happens? Thus, reducing the amount of serotonin synthesis should only cause a decrease in neurotransmission when the reserves in the vesicles are depleted.

So what gives? Astonishingly this is not explained in the literature I have found.

# Answer
> don't the neurons already have plenty of serotonin stored in the axon vesicles from which the neurotransmission happens

Sure, but neurotransmission is happening all the time. It's not uncommon for a neuron to fire several times a second, and though not nearly every vesicle is released per action potential, over minutes to hours you should be thinking about hundreds to tens of thousands of possible release events.

Of course, neurotransmitters aren't simply released and then gone; monoamine transporters are particularly famous drug targets; these transporters facilitate reuse of neurotransmitters as well as their degradation.

I had a bit of trouble finding a solid estimate of brain half-life/turnover of serotonin in papers I have access to, though this paper used an indirect method by using an inhibitor of subsequent serotonin metabolism:

*Udenfriend, S., & Weissbach, H. (1958). Turnover of 5-hydroxytryptamine (serotonin) in tissues. Proceedings of the Society for Experimental Biology and Medicine, 97(4), 748-751.*

> Such estimates indicate a half-life in brain of the order of minutes

Other papers like this one:

*Diaz, P. M., Ngai, S. H., & Costa, E. (1968). Factors modulating brain serotonin turnover. In Advances in pharmacology (Vol. 6, pp. 75-92). Academic Press.*

refer to

> Reports in the literature show that the turnover time of brain NE stores is 5.8 hours and that of brain 5-HT stores is 1.2 hours

but I don't have access to the full-text to find what reference they refer to. However this seems consistent with the timeline of tryptophan depletion (over several hours, or days) referred to in papers like this one:

*Nutt, D. J., Forshall, S., Bell, C., Rich, A., Sandford, J., Nash, J., & Argyropoulos, S. (1999). Mechanisms of action of selective serotonin reuptake inhibitors in the treatment of psychiatric disorders. European neuropsychopharmacology, 9, S81-S86.*
> 3 votes

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Tags: neuroscience, neuro-transmitters, experimental-neuroscience, serotonin
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title: What is Incestuous Resistances?

text:
# Question
Title: What is Incestuous Resistances?
The context of the question is given below:

> As she preferred to follow the hidden presentiments of puberty rather than her duties towards the school and her teacher, she allowed her libido to fall on the little boy, from whom, as we saw, she awaited some mysterious advantages. Even if analysis had demonstrated it as a fact that **she had had incestuous resistances against her teacher on account of the transference of the father-image**, those resistances would only have been secondary phantasies, that had become inflated.
>
> -THE ANALYSIS OF THE TRANSFERENCE, page 132, The Theory of Psychoanalysis, By C. G. JUNG (NERVOUS AND MENTAL DISEASE MONOGRAPH SERIES, No. 19, Nervous and Mental Disease Publishing Co., New York, 1915).

I am trying to get a clear idea about why or how this "incestuous resistances against her teacher" is created, it is not clear to me, though the author added" on account of the transference of the father-image", so what if the transference of the father-image happens? I would like to understand that a bit more explicitly/elaborately (**based on what is written on the book**).

**My interpretation:**

"Incestuous resistances" is caused to resist incestuous fantasy/thinking. Since incest is bad, any person who brings the idea of incest in patient's mind, will be/is resisted by the patient as incest is not accepted socially

> ...It almost looks as if the Œdipus-complex would develop into consciousness if **the development of the child were to go on without restraint and if no cultural tendencies influenced it**. ...that the incest-barrier is **the result of experience, of the selective influence of reality,** (Page 71)

thus though patient is thinking about incest, at the same time due to the possibility of becoming social-outclass, the person associated with incest intimidates the patient, thus "incestuous resistances against" a person is created.

Is this interpretation correct? If not, please do make it right, thanks.

# Answer
As highlighted before, whilst I am a defender of Freudian and Neo-Freudian psychology, please be aware that this covers areas of psychology considered by some here to be pseudoscientific

---

The basis of incestuous resistance in this context is described from page 70 of *The Theory of Psychoanalysis* by Carl Jung (Nervous and Mental Disease Publishing Co., New York 1915) available in PDF from https://archive.org/download/theoryofpsychoan00jungiala/theoryofpsychoan00jungiala.pdf

> Freud has a special conception of the incest-complex which has given rise to heated controversy. He starts from the fact that the Œdipus-complex is generally unconscious, and conceives this as the result of a repression of a moral kind. It is possible that I am not expressing myself quite correctly, when I give you Freud's view in these words. At any rate, according to him the Œdipus-complex seems to be repressed, that is, seems to be removed into the unconscious by a reaction from the conscious tendencies. It almost looks as if the Œdipus-complex would develop into consciousness if the development of the child were to go on without restraint and if no cultural tendencies influenced it. Freud calls this barrier, which prevents the Œdipus-complex from ripening, the incest-barrier. He seems to believe, so far as one can gather from his work, that the incest-barrier is the result of experience, of the selective influence of reality, inasmuch as the unconscious strives without restraint, and in an immediate way, for its own satisfaction, without any consideration for others. This conception is in harmony with the conception of Schopenhauer, who says of the blind world-will that it is so egoistic that a man could slay his brother merely to grease his boots with his brother's fat. Freud considers that the psychological incest-barrier, as postulated by him, can be compared with the incest-taboo which we find among inferior races. He further believes that these prohibitions are a proof of the fact that men really desired incest, for which reason laws were framed against it even in very primitive cultural stages.

The child is seeing their father within the teacher, and with this projection of the father figure onto the teacher, the child is developing the Oedipus complex (sexual desire of the child to their opposite sex parent, according to Freud). This Oedipus complex is creating an unconscious resistance to learning as the attentions toward the teacher are more of a romantic nature rather than a teacher/schoolchild nature.
> 3 votes

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Tags: sexuality, psychoanalysis, jung, freud
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title: Non-serotonergic hallucinogens

text:
# Question
Title: Non-serotonergic hallucinogens
According to this article, agonism of the 5-HT$\_{2A}$ is necessary for hallucinogenesis. Now, not all hallucinogens are primarily serotonergic, but does there exist hallucinogens that aren't at all serotonergic? If so, that means there are hallucinogens that don't agonise the necessary receptors for hallucinogenesis.

Would that mean that these non-serotonergic hallucinogens only produce visual distortions (illusions), and not "proper" hallucinations? And do all serotonergic hallucinogens activate the 5-HT$\_{2A}$ receptors, or are there serotonergic hallucinogens that don't activate exactly this receptor, but still primarily or partially operates on all the other serotonergic receptors?

# Answer
> -1 votes
I am not a scientist, just an ordinary person who has done a lot of reading on this subject. I will state what I believe to be true based on this reading. Please note that I am totally blind and using a speech to text dictation function on my phone to write this comment, so apologies in advance for any grammatical and spelling errors. I have tried to correct what I can and I hope you enjoy reading this and benefit from it. The term psychedelic has Greek origin and means mind manifesting. Psychedelic most properly refers to classical psychedelics otherwise known as serotonergic hallucinogens. These drugs strongly activate the 5HT2A receptor and this action is both necessary and sufficient for these drugs to generate the majority of their effects. As mentioned in a previous comment, classical psychedelics should be considered as a distinct category within the class of hallucinogens but I want to add that they should be separated more on the basis of their unique effects rather than simply their receptor pharmacology. To put it simply, 5Ht2A receptor activation is absolutely necessary for classical psychedelics to generate The whole range of their well-known and common effects. However, there are many other classes of hallucinogens that act on different receptor targets and have no detectable effects on any type of serotonin receptor including 5HT2A. NMDA antagonist (PCP and ketamine), anticholinergics(Scopolamine and diphenhydramine) and The kappa opioid agonist including the notoriously powerful naturally occurring atypical disassociative hallucinogen Salvinorin A. These hallucinogens act on receptors that have nothing to do with serotonin and I think this has some interesting outcomes in terms of user experiences. Unfortunately I only managed to find very little information on the subject of the link between receptor pharmacology and types of hallucinations generated. However, the overall idea I got from reading user experiences was The following. Classical psychedelics are by far the most potent in altering human consciousness. Whilst they create visual effects and may produce many types of hallucinations that range in intensity I think the most profound effects are on a persons sense of identity, perhaps they generate hallucinations of emotion in addition to those affecting the traditional five senses. Therefore, whilst you may hear, see, smell and even taste things that are not really there, on psychedelics, most of your attention will probably be focused on questioning your identity and life choices or reflecting on the nature of the universe and your place within it. Similar in some respects to the classical psychedelics, The kappa opioid agonist Salvinorin A as well as synthetic kappa opioid agonist ligands, produce a range of hallucinatory experiences, perceptual alterations and emotional changes which increase in intensity in a dose dependent manner. These drugs also share a strong emphasis on consciousness and identity/ego with the classical serotonergic psychedelics. Nevertheless, they carry a strong disassociative and often dysphoric component and are much more likely to cause out of body experiences and derealisation. The NMDA receptor antagonists are in my opinion One of the most interesting hallucinogens because they have the most recreational value. Often referred to as “disassociative anaesthetics“, they are capable of producing true hallucinations but these usually occur in a strange State of altered consciousness known as disassociative anaesthesia. Some people have theorised that this might involve a disconnect between the body and sensory input coming from it and the brain/mind making it a form of chemically induced sensory deprivation. However, I think the more correct opinion is that blockade of NMDA receptors on inhibitory interneurons leads to excessive glutamate release in other parts of the brain and resulting in an excitatory/inhibitory imbalance with the consequence of deranged information-processing in the brain. NMDA antagonists are renowned for their ability to frequently induce severe perceptual distortions, vivid dream like hallucinations, and even out of body experiences along with derealisation. I’m not sure as to why NMDA antagonists have greater recreational value than most other hallucinogens, but some interesting suggestions include a propensity to produce euphoria due to significantly high dopamine release, The numbing effect of the disassociative/anaesthetic effects on negative emotions especially in people liable to use drugs to escape their current reality and finally a possible antidepressant effect that may produce a mild mood lift known as an afterglow once the experience has worn off. Finally, the anticholinergics A.k.a. delirients are the drugs most likely to produce true/highly realistic hallucinations that are in most cases completely indistinguishable from reality. Even more worryingly, many of these hallucinations are reportedly reflections of what may happen in real life. For example, whilst in some cases you may see and feel spiders/other insects crawling all over you, in other cases users have invited friends into the house, eat with them and conversed with them for a very long period of time only to later discover that no one was actually there. Anticholinergics also come with a range of incredibly unpleasant side-effects including high body temperature, severely dry mouth, constipation, urinary retention, high blood pressure, rapid heartbeat, severe memory loss, dizziness, unconsciousness and possibly death.

I’ve never tried a hallucinogen in my life and I don’t ever intend to try one. However, out of all hallucinogens the class I would stay the furthest away from and would not even touch with a 10 foot pole are the classical serotonergic psychedelics. Whilst this might surprise you given that classical psychedelics are ranked amongst the safest drugs in terms of social and physical harm and given that they lack addictive qualities, I feel that their ability to profoundly alter human consciousness and shatter one’s identity with possible permanent consequences far outweighs their physical safety profile. Whilst there are many things about myself I wish to change or improve, I don’t believe the correct way is to take a sledgehammer and smash my identity to pieces through a chemically induced and uncontrollable mind-bending experience that could leave me traumatised and suffering with anxiety and depression that I never had before. I’ve seen this reported many times before, but psychedelic enthusiasts seem to shove it under the carpet and blame The user for failing to surrender to the experience or learn from it and understand its message correctly.

Now I will leave you with something that is confusing yet equally interesting. As I have mentioned above, I am blind so I can’t post links to Scientific studies but you could probably find them easily on the Internet. Basically I have read contradicting articles that examined the role of certain receptors in hallucinations. Whilst many of them supported what I have stated above, others have suggested that whilst 5HT2A receptor activation is necessary for the effects of classical psychedelics but not directly for the effects of other hallucinogens, blocking 5HT2A receptors with potent antagonist could suppress hallucinogen associated behaviours in animals injected with kappa opioid agonists. I don’t know what to make of this finding, however it might well be that large-scale and potent blockade of 5HT2A receptors might have a general calming/antipsychotic affect on the brain that intern suppresses hallucinations. If this is the case, then there’s really not much contradiction but it’s very interesting nonetheless. I also read a study in the journal frontiers which explained that the mild disassociative component of The Serotonergic empathogen MDMA was not at all dependent on the 5HT2A receptor as previously suspected. I’m going to read that study again because I can’t remember whether they pointed out a different target and what the implications could be but I would be happy to post what I have learnt if any of you are interested.

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Tags: hallucinations, optical-illusion, serotonin, psychedelics, cognitive-distortion
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# Question
Title: Do alpha waves vanish when I open my eyes in a dark room?
Alpha brain waves show up in your EEG when you close your eyes.

Do they vanish when I open my eyes in a dark room? To put it in a different way: Is it necessary to have your eyes shut or that you don't see anthing?

# Answer
Yes they do.

That is to say, light conditions do not generally affect alpha waves, only the eyelids do (and other factors). This has led to alpha waves being interpreted as reflecting an active inhibitory process in the visual cortex (relaxation) rather than a reduction of stimulus (resting).

The following image is from an Israeli study published in 2013 called "The dark side of the alpha rhythm": Notice how all the graphs show no significant difference between light and dark conditions in both eyes open and eyes closed cases.

Mounting evidence from studying blinking, saccades, and stimulating the retina from behind the eyelids (through the oral cavity) suggests that closing the eyes initiates an inhibitory process that actively blocks visual processing (rather than passively relying on darkness), so darkness is not necessary, only shutting the eyes is sufficient.
> 8 votes

# Answer
No, **they do not vanish**. But when you open your eyes the alpha waves **decrease in amplitude** in a dark room to about the same extent as if you were in a well-lit room.

See @ArnonWeinburg's answer. The following graph from an article at Sapienlabs.org ("Eyes Open, Eyes Closed and Variability in the EEG") is also instructive. As you can see, alpha waves do not "vanish" when a person's eyes are open:
> 3 votes

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Tags: eeg, brain-waves
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# Question
Title: What happened in the fifth year of the girl that made her afraid of her father in the book "The Theory of Psychoanalysis"?
The case in question is that of an intelligent girl of eleven years of age, of good family. Dr. Jung starts discussing her in his book, on page 113 ("A CASE OF NEUROSIS IN A CHILD"), at one point he wrote:

> These sexual tendencies have caused the fear of the father. Still, we must not forget that she had this dream in her fifth year. At that time these sins had not been committed. Hence we must regard this affair with the other girls as a reason for her present fear of her father; **but that does not explain the earlier fear.** But still, we may expect it was something of a similar nature, some unconscious sexual wish, corresponding to the psychology of the forbidden action previously mentioned. The moral value and character of this wish is even more unconscious with the child than with adults. To understand what had made an impression on the child, **we have to ask what happened in her fifth year. Her youngest brother was born at that time. Even then her father had made her nervous.**
>
> -THE ANALYSIS OF THE TRANSFERENCE, page 121, The Theory of Psychoanalysis, By C. G. JUNG (NERVOUS AND MENTAL DISEASE MONOGRAPH SERIES, No. 19, Nervous and Mental Disease Publishing Co., New York, 1915).

But I never found on the book what happened in her fifth year that made her afraid of her father, why or what, in her fifth year - when her youngest brother was born Even then - her father had made her nervous?

# Answer
> -1 votes
Mostly, Jung is making stuff up based on an unfounded assumption that we can best understand kids by assuming they have sexual fantasies about their parents and that most things that are wrong with them are because these fantasies are somehow unresolved.

Jung's theory about girls is called Electra complex, based on Freud's Oedipus complex (originally applied to boys, though also expanded to include girls; Freud disagreed with Jung that they should be named separately).

As written in Wikipedia:

> There is very little scientific evidence for the reality of the Electra complex. The predictions of the theory are not substantiated by experiment.\[21\]\[22\] The Electra complex is not widely accepted among modern mental health professionals and is not listed in current versions of the Diagnostic and Statistical Manual of Mental Disorders.\[23\]

Earlier in the book, Jung talks about a dream the girl had:

> At the third interview the little girl related a dream she had had when she was five years old, and by which she was greatly impressed. She says, " I'll never forget this dream." The dream runs as follows : " I am in a wood with my little brother and we are looking for strawberries. Then a wolf came and jumped at me. I took to a staircase, the wolf after me. I fall down and the wolf bites my leg. I awoke in terror."

In your quote, "she had this dream in her fifth year" is referring to this dream. Jung says this sounds like the "well-known German fairy-tale of Little Red Ridinghood, which is, of course, known to the child". He goes on to talk vaguely about a broader astro-mythological context to fairy tales and mythology and then jumps to:

> These currents are caused by the libido in its unconscious forms. The material which comes to the surface is infantile material, hence, phantasies connected with the incest-complex.

Jung has no evidence for this, Freud has no evidence for this, they just *say it* and then start *interpreting everything as based on this*, kind of like a conspiracy theorist would. It's an absolutely terrible way to go about actually understanding the world, and not at all how science works.

Other statements seem a bit more believable at face value:

> The fear of the wolf in the dream is therefore fear of her father. The little patient explains her fear of her father by his severity towards her. He had also told her that we only have bad dreams when we have been doing wrong.

Basically, her father is "severe" towards her - maybe that means he yells at her, maybe it merely means he is strict about her behavior, maybe it means he is physically imposing or abusive; the details are not given. But it seems he has told his young daughter that if she has bad dreams it means she's doing something wrong; I can imagine that making a kid feel pretty uncomfortable by itself. What Jung thinks is more important than that, though, is this sexual obsession she has with her father.

As far as what *happened* to her in her fifth year? It's right in your quote:

> Her youngest brother was born at that time

He elaborates:

> This dream illustrates the first impressive appearance of the sexual problem, obviously suggested by the recent birth of the little brother, just such an occasion when experience teaches us that these questions become vital.

So in other words, Jung says girls are sexually obsessed with their fathers, "obviously" having a sibling born surfaces these obsessions, and so all this trouble has magnified around when the girl is 5.

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Tags: developmental-psychology, fear, psychoanalysis, jung, children
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# Question
Title: Curt Richter's rat hope experiment: Why did the first nine rats survive for days?
I can understand the part that the experimenter saved the rat just before it was about to die and then the rat lasted longer for the next drowning. But I do not understand what it means that before such intervention, when he first tried drowning, first 3 rats died in 2 minutes but the remaining 9 rats survived for days.Was it just a random chance that the first 3 rats happened to have little hope and the remaining 9 rats had naturally more hopes?

> The first rat, Richter noted, swam around excitedly on the surface for a very short time, then dove to the bottom, where it began to swim around, nosing its way along the glass wall. It died two minutes later. Two more of the 12 domesticated rats died in much the same way. **But, interestingly, the nine remaining rats did not succumb nearly so readily; they swam for days before they eventually gave up and died.** ..... Richter then tweaked the experiment: He took other, similar rats and put them in the jar. Just before they were expected to die, however, he picked them up

https://www.psychologytoday.com/gb/blog/kidding-ourselves/201405/the-remarkable-power-hope

# Answer
For more information on the experiment, there is Swamy (2020):

> The conclusion drawn was that since the rats BELIEVED that they would eventually be rescued, they could push their bodies way past what they previously thought impossible.

and the source (Richter, 1957) can be downloaded in PDF

I had to re-read the Richter paper a couple of times to digest it, and from my understanding, the differences in swimming time was in the same (first) experiment. The tweak to the experiment was where, instead of using domesticated rats, they used hybrid rats ("crosses between domesticated and wild rats").

## References

Richter, C. P. (1957). On the phenomenon of sudden death in animals and man. *Psychosomatic Medicine, 19*, 191–198. https://doi.org/10.1097/00006842-195705000-00004

Swamy, S. (2020). The Power of Hope: A Rat Experiment by Dr Curt Richter. *LinkedIn* https://www.linkedin.com/pulse/power-hope-rat-experiment-dr-curt-richter-santosh-swamy
> 3 votes

# Answer
**It's not clear what caused this.** This variation in swimming times is in fact what motivates Richter to continue tweaking his experiment:

> The significance of this average curve was greatly reduced by the marked variations in individual swimming times. At all temperatures, a small number of rats died within 5 - 10 minutes after immersion, while in some instances others apparently no more healthy, swam as long as 81 hours. The elimination of these large variations presented a real problem, which for some time we could not solve. Then the solution came from an unexpected source - the finding of the phenomenon of sudden death, which constitutes the main topic of this communication.

The numbers you cite regarding the 3 versus 9 rats comes from his second run of the experiment where he tests whether trimming the whiskers in the rats would result in different times.

> The first rat swam around excitedly on the surface for a very short time, then dove to the bottom, where it began to swim around nosing its way along the glass wall. Without coming to the surface a single time, it died 2 minutes after entering the tank. Two more of the twelve domesticated rats tested died in much the same way; however, the remaining 9 swam 40 to 60 hours.

It seems that it was just caused by random luck.

### References

Richter, C. P. (1957). On the phenomenon of sudden death in animals and man. *Psychosomatic Medicine, 19*, 191–198. https://doi.org/10.1097/00006842-195705000-00004
> 1 votes

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Tags: experimental-psychology, animal-cognition
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# Question
Title: What makes pathological demand avoidance different from reactance?
I learned about the term reactance after some research, what wasn't as obsessive in the description as I had observed with some people in the past. Still made a very good point in describing the behavior and its triggers I was looking for.

Just coincidentally I learned a few days later about pathological demand avoidance. And while I understand it that way, that the former is more like a behavior everyone is driven by, to different strong extends. And the latter having additional symptoms beside this leading to more obsessive behavior and generally an more present impact than what I understand reactance to be like. But focusing on the core, I wonder what they are different in, if anything. As both boil down to feeling resistant to choose options you feel being obligated to choose.

So is PDA actually just a strong form of reactance reinforced by possibly other (autistic) traits? Or do they have a distinct difference in their core definition of affecting someone?

# Answer
So, reactance seems to be specific to things that are attempting to alters one's autonomy or choices. PDA is when our brain sees any action we are trying to take as a danger, so it makes us avoid that action by any means possible. PDA is our brain trying to keep us safe from perceived harm. With PDA, demands can be anything, including things that trigger reactance, but also things we want to do such as hobbies, and our basic bodily needs such as eating and sleeping. PDA itself can actually cause reactance because we feel unable to have control over what we do, we can feel powerless against our demand avoidance. It's not the demand itself that causes reactance for PDAers, but our PDA which won't let us do these demands.
> -1 votes

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Tags: social-psychology, autism
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# Question
Title: Are many anticonvulsants just coincidentally also psychoactive?
Many of the antiseizure I'm aware of are described as having the potential for behavior altering side-effects. I am curious about this.

* Is there something about the chemistry of the brain that frequently makes anticonvulsants also psychoactive? Does it have to be this way?

OR

* Maybe the anticonvulsant drug profiles are like this because much more money is invested in R&D for psychoactive drugs used in psychology than is invested in R&D for epilepsy drugs. And, during the R&D process the anticonvulsant property of a drug is discovered as being the *side effect* of the drugs whose main property is psychoactivity. And this might be why the anticonvulsants being sold are psychoactive?

Viagra was discovered during R&D into high blood pressure. Viagra **does** lower high blood pressure. Viagra **also** has a side effect. People take Viagra for the side effect.

So, might it be like:
During R&D into psychoactive drugs, Zonisamide was discovered to have the side effect of elevativing the seizure threshold. Zonisamide **is** psychoactive. Zonisamide **also** elevates the seizure threshold as a side effect. People take Zonisamide for the side effect?

Is it understood why anti-epileptic drugs are always mood altering? Is it chemical? a product of the R&D cycle? a simple correlation that a person with the disease might be more emotional?

# Answer
Note: I have epilepsy, and have been taking anticonvulsants for the best part of 2 decades. I've stumbled across this post after researching some things related to recent changes in side-effects, dosage, and other issues that stem from my treatment plan.

## Are they coincidentally psychoactive?

No. Absolutely not. By definition, every anticonvulsant drug *has* to be psychoactive. I noticed that Chris Rogers in a comment mentioned Felbamate as the only non-psychoactive drug. I want to address this directly and say that Felbamate most definitely fits the cited description of a psychoactive substance:

> a chemical substance that changes nervous system function, and results in alterations in perception, mood, consciousness, cognition, or behavior

Just like any other anticonvulsant, felbamate relies on GABA and GABA receptors to do its job. GABA (or gamma aminobutyric acid) is the main inhibitory neurotransmitter. Its primary role is to reduce excitability of neurons. Now let's clarify what a seizure actually is:

A seizure is the hyper-excitability of neuron(s) that trigger hyper-synchronisation of surrounding neurons, resulting in something akin to a neurological Kessler syndrome where (over simplified): a single neuron gets hyper excited, and triggers an ever larger group of surrounding neurons to join in and fire at the same time. If that happens in your motor cortex, that can lead to most of the muscles in your body to contract and relax at the same time (ie a tonic-clonic seizure).

All anticonvulsants rely on GABA to reduce the excitability of neurons to prevent these cells from triggering your neurons into this mexican wave type of firing. No medication exists that specifically targets the neurons that are hyper-excitable, though, and thus there isn't an anticonvulsant out there that doesn't list any of the following side effects:

* Drowsiness
* Fatigue
* Memory loss
* Brain fog
* Depression
* Suicidal thoughts
* Weight gain

Like many people with epilepsy, I often describe the effects of the medication as "feeling suppressed". It's as though I've not slept for 24 hours. Like a severe lack of sleep, it definitely impacts things like mood, cognition, consciousness, and even perception. My perception of time, for instance, is absolutely not the same as it was before I went on medication. The medication-induced feelings of depression are very real, too. The inability to perform physical tasks with the precision, speed, and energy that comes natural to any human being just isn't there anymore. Your metabolism is impacted (hence weight gain is a common complaint), and so on...

In addition to this, most of these meds have an effect on endocrine hormone production/regulation, which in turn either reinforces mood/behaviour changes, or causes a slew of new ones.

I recently tried to switch to a new treatment plan, and moved to a high dose of levetiracetam (keppra). A side effect of this is affectionately known as "kepprage". The leaflet in the box just calls it "aggression/assertiveness". While the specifics about how levetiracetam exactly works is (AFAIK) not fully understood, I found a paper a while back specifically looking into the causes of behavioural changes. The neuro-chemistry of this drug has some remarkable similarities to steroid abuse. source

All in all: when talking about anticonvulsant medication, we're talking about drugs that work because they regulate/alter the functioning of your central nervous system. That's the first half of the definition of psychoactive as cited above. Because their job is to reduce excitability of neurons, they all (AFAIK) use GABA in some capacity to do their job. This, by definition, will have an effect. The bare minimum is that you'll feel tired, but more often than not (AFAIK, always), it'll impact your ability to focus, remember things, and very commonly will make people feel more down (mood changes). Feelings of depression, fatigue, and confusion, combined with memory loss will result in behavioural changes. TL;DR **all** anticonvulsants are, by definition psychoactives.

## Is the anticonvulsant effect a side-effect?

This is a bit more of a grey area. Sodium valproate (or valproic acid) was first synthesised in the late 19th century, and for 80 years, it was uniquely used as a "metabolically inert" organic solvent. Its anticonvulsant effects were accidentally discovered, and the drug has since seen ever more medical applications (epilepsy treatment, bipolar disorder, schizophrenia treatment, etc...). wiki:

> Valproic acid was first synthesized in 1882 by Beverly S. Burton as an analogue of valeric acid, found naturally in valerian. Valproic acid is a carboxylic acid, a clear liquid at room temperature. For many decades, its only use was in laboratories as a "metabolically inert" solvent for organic compounds. In 1962, the French researcher Pierre Eymard serendipitously discovered the anticonvulsant properties of valproic acid while using it as a vehicle for a number of other compounds that were being screened for antiseizure activity. He found it prevented pentylenetetrazol-induced convulsions in laboratory rats. It was approved as an antiepileptic drug in 1967 in France and has become the most widely prescribed antiepileptic drug worldwide. Valproic acid has also been used for migraine prophylaxis and bipolar disorder.

So in a way, sodium valproate became an anticonvulsant as its use in treating epilepsy was an unintended side-effect. Then again, its initial use was not one of a psychoactive drug either.

Levetiracetam, on the other hand, was a more recently developed drug that, as far as I know, was specifically developed to be used as an anticonvulsant. It is a psychoactive, so it's not a stretch to assume that the R&D that lead up to its discovery was focused on psychoactive compounds, but the end product was clearly not a psychoactive drug that just so happened to have anticonvulsant properties. Its an anticonvulsant by design that just happens to have psychoactive properties.

From my own experience, I can also say that its psychoactive properties are pretty damn terrible. When I was on a high dose of the stuff, I had an episode where I screamed at my girlfriend, threw stuff around, and just raged for extended periods of time. When I woke up the next day to find her packing, I asked what was going on. I had no recollection of the incident. Naturally, I immediately got in touch with my neurologist and changed my treatment plan.

## Serendipity and R&D

All this, of course, is not to say that there aren't psychoactive drugs that are developed, and then found to have anticonvulsant properties. However, the opposite is just as common. Again: sodium valproate started out as a solvent, was repurposed as an anticonvulsant, is now used to treat things like bipolar disorder, anxiety disorders, migraines, and I know people personally who have received it as part of their treatment for schizophrenia and narcolepsy.

The one thing these conditions have in common is that they are, at least physiologically speaking, neurological in nature. It stands to reason that any substance that effects the central nervous system represents an a potential use-case to explore. That's why things like levetiracetam are currently being evaluated as potential treatments in patients with Alzheimer's and Parkinson's disease.
> 3 votes

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Tags: psychopharmacology, drugs, epilepsy
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title: Why Is It Still Called Schizophrenia?

text:
# Question
Title: Why Is It Still Called Schizophrenia?
> Schizo = Split
> Phrenia = Mind
> The word schizophrenia translates as splitting of the mind, its use was intended to describe the separation of function between personality, thinking, memory, and perception.

Japan changed this disorder's name to `integration disorder` in 2002, and South Korea changed it to `attunement disorder` in 2012. Does splitting of the mind describe the disorder appropriately enough to be used as the medical term, and how so? How would the aforementioned functions be separated in schizophrenics?

# Answer
> 2 votes
Lots of terms live long beyond their etymology, in science and outside. Etymology is really about *history* of language, not *meaning* of language: knowing where a word originated does not tell you how it is actually used now.

For another example, consider "dinosaur" which originated as "terrible lizard"; dinosaurs are of course *not* lizards, and there is little sense in which they are *terrible* as a group. That doesn't matter much, though, because the meaning of the word has evolved substantially since it was coined, and it certainly can be used separate of its etymology. In other cases, like the term "big bang", the misleading aspects of the term seem to be detrimental to understanding by a lay audience, yet that term persists as well.

I think "schizophrenia" is more like "dinosaur". I don't think that many people who use the word "schizophrenia" are mentally breaking it up into its Greek origins to describe a split mind, they're using it to describe a particular psychiatric condition with all the aspects and variations learned since the term was coined. Renaming schizophrenia would require that everyone who uses the new term also needs to know the old term, because every paper, textbook, medical chart, etc, from before that change will use the old term. There is a lot of inertia to language.

That doesn't mean it's impossible to rename a disorder. For example, there has been more movement towards renaming psychological disorders that come to have derogatory meanings, for example the old term "mental retardation" is rarely used now except in old texts. Clinicians need to be able to communicate in medical terms with their patients and their parents. There certainly are some movements to rename schizophrenia, but they seem to come primarily from *this* perspective of stigma, rather than one of etymology. For example:

Gaebel, W., & Kerst, A. (2019). The debate about renaming schizophrenia: a new name would not resolve the stigma. Epidemiology and psychiatric sciences, 28(3), 258-261.

My understanding is that in places where schizophrenia has been renamed that you give as examples, renaming has occurred because the term used in those languages had a modern, misleading meaning in those languages. It would be like if the English term were precisely "split mind disorder" or something like that. Modern speakers don't use the Greek elements of the word schizophrenia independently. Some other words may share similar roots, but it's just not familiar to an ordinary speaker. If they do know the meaning of "schizo" or "phrenia", it's most likely because they read a textbook or article about the origins of the term schizophrenia, or one of a few other handful of medical terms ("phrenic" comes up occasionally in anatomy; "schizo" shows up elsewhere in psychology/psychiatry).

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Tags: terminology, schizophrenia, analysis, terms
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# Question
Title: What are these extra 11 dimensions of human mind?
I posted this question on the physics stack exchange, but I was guided to ask the question here though from the view point of a neuro-scientist which should be more useful if she has already followed the general current of changes in Theoretical physics:

Recently I faced a research result showing the brain works in 11 dimensions. I was wondering if these dimensions have anything possible to do with those of M-theory?

They use algebraic topology techniques to come up with their result.

In string theory there are 3+1+6+1 dimensions, space+time+compactified dimensions+extended dimension on the strings(strings change into branes)

Cliques of Neurons Bound into Cavities Provide a Missing Link between Structure and Function

# Answer
No, there's no relationship to string theory.

You might imagine brain activity as taking place in an N-dimensional space, where N is the number of neurons in the brain. However, neurons aren't independent of each other, so there aren't really N unique dimensions. Using various dimensionality reduction techniques, for example principle component analysis, you can choose to discard some dimensions that have less variance and if you set some threshold you can say "well really there are X dimensions of brain activity". Of course that number is dependent on the threshold you choose.

The actual meaning of those dimensions varies by the approach taken, but here I think the closest would be that the 11 dimensions represent different functional networks in the brain doing different things. Functional meaning they do similar things at the same time.

Other people get different numbers so 11 is just their particular result, there's nothing special or consistent about 11.
> 3 votes

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Tags: consciousness, psychophysics
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# Question
Title: What does "all-or-nothing" means in spiking neural network?
I'm reading a paper by Auge et al. (2021). In the introduction they said "Spiking Neural Networks (SNNs) use short 'all-or-nothing' pulses to encode and transmit information".

I'm not sure what is the meaning of "all-or-nothing" in this context. Does it mean binary?

Auge, D., Hille, J., Mueller, E., & Knoll, A. (2021). A survey of encoding techniques for signal processing in spiking neural networks. Neural Processing Letters, 53(6), 4693-4710.

# Answer
> 1 votes
For an artificial network, yes, it typically means there is a binary **output**; this is a standard neuron model.

For a biological network, it's a bit more complicated, because although any moment in time can be a "spike" or "no spike", there isn't some discrete timeseries described by a binary code, but rather single events with an occurrence time.

# Answer
> 1 votes
I guess it comes from physiology where the strength of the response of a neuron or muscle fiber doesn't have anything to do with the strength of the stimulus. If a stimulus is above a certain threshold, the neuron will fire. So, in terms of SNN, it seems to me like a binary coding, where a neuron is either active or inactive within a specific time interval.

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Tags: neuroscience, neural-network, artificial-intelligence
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# Question
Title: How to evaluate the convergence of a staircase?
I have a 2AFC staircase, with transformed up and down method (2up 1 down) or (2down 1 up), with equal step size (at the beginning there are higher step sizes, at the end there are the lower value). This staircase will be used for detecting the performance of the subjects in a sustained attention task.

I know from the literature that the 2up 1 down staircase should converge at the 70% point of the pychcometric function. But how can I test this? When a subject has done the staircase and I obtain his threshold level, how can I test if this threshold level is equal to a performance of 70%?

How Can I evaluate if the staircase worked properly?

# Answer
> 3 votes
A staircase is an adaptive procedure. To test whether its outcome is correct you can do the math (*e.g.*, Levitt (1971); Zwislocki & Relkin (2001)) by calculating what a 2-up, 1-down method converges to. Note that according to Zwislocki & Relkin, the 2-up, 1-down procedure results in 71% correct rate at threshold (70.7%, to be precise), and not 70% as you claim. That latter PNAS paper has been most enlightening to me by the way.

Alternatively, you can put the math to the test by taking your stimulus level at threshold, and measure the %correct score using the method of constant stimuli (non-adaptive). That should come down to a correct rate of 71%. Learning effects and test/re-test variability might mess it up though.

<sub>**References**
**-** Levitt, *JASA* (1971); **49**(2-2): 467-77
**-** Zwislocki & Relkin, *PNAS* (2001); **98**(8): 4811-4</sub>

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Tags: neuroscience, cognitive-neuroscience, measurement, methodology, psychophysics
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# Question
Title: Is anyone here familiar with techniques and/or equipment for performing cerebrospinal fluid transfusions?
I am a student at a University and we are discussing putting together a lab assessing the benefits that may be associated with cerebrospinal fluid (CSF) transfusions in Alzheimer's disease mice. So far it looks like from this paper there may have existed a device at one time that could have been modified for our purposes. I contacted Infors AG and the representative believes this device to be out of production. Does anyone here know of anyone who is doing work with CSF transfusions? We are very eager to begin, especially myself and would greatly appreciate any leads as to literature available on this technique or biotech companies that may be able to provide the tools we seek.

# Answer
> 0 votes
The methods section of Young CSF restores oligodendrogenesis and memory in aged mice via Fgf17 should cover this (Published May 11, 2022).

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Tags: experimental-neuroscience
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# Question
Title: Understanding the difference between stress and anxiety with goal directed behaviour
I'm currently writing a paper and one of the points is about cognitive performance being impeded on in general anxiety disorder patients.

The issue I have is that I found a great paper:

> The stressed prefrontal cortex and goal-directed behaviour: acute psychosocial stress impairs the flexible implementation of task goals
>
> https://www.psychologie.uni-freiburg.de/Members/kiesel/Publications/PlessowKieselKirschbaum2012EBR.pdf

that has identified how stress hinders cognitive flexibility.

At the same time though the consensus, drawn by another paper is that

> Experimentally induced and real-world anxiety have no demonstrable effect on goal-directed behaviour
>
> https://www.researchgate.net/publication/339629155\_Experimentally\_induced\_and\_real-world\_anxiety\_have\_no\_demonstrable\_effect\_on\_goal-directed\_behaviour#pfc

Basically one papers points out that stress works against cognitive flexibility and goal directed behaviour, while anxiety seems to have no effect. The acute anxiety paper references the stress paper, suggesting their findings are complementary rather than mutually exclusive.

Im not sure how this can make sense, aren't anxiety and stress co-occuring phenomena in GAD?

# Answer
I think you need to be clear about the terms you are using:- Stress describes the feeling of pressure we experience in meeting the demands made upon us, everyone is dealing with multiple stressors all the time, its what keeps us moving. If it wasn't for stress (the demands) we wouldn't get up in the morning. Its possible when people are faced with lots of stressors that they can overwhelm a persons coping resources. Anxiety is different, its the feeling we experience when faced with a perceived threat, its a cognitive state, we call dealing with actual threat, fear. All feelings have a function, they motivate certain types of behaviour, with stress we are motivated to manage or remove the cause, we even get pleasure, a sense of achievement when we are successful. With things outside of our control or skills, we can get stuck in ineffective problem-solving and it can lower mood. Stress by definition requires some form of adaptation to successfully manage it. Anxiety "captures" our cognitive resources, we focus our attention on the perceived threat and it significantly biases our thinking. It motivates escape or safety behaviours, for example a person having a panic attack usually thinks they are at immediate threat of dying and experience extreme physical symptoms that support this. I have to say I think your second reference bordered on the bizarre, to claim that they have no effect of behaviours, effectively dismisses the theoretical frameworks of emotions, all the research in the clinical management of anxiety and centuries of human experience.
> -1 votes

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Tags: behavior, stress, anxiety
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# Question
Title: The bystander effect depends on various variables, most of which don't necessarily require the present of other people. Why is it defined so?
From Bystander effect - Wikipedia:

> The bystander effect, or bystander apathy, is a social psychological theory that states that individuals are less likely to offer help to a victim when there are other people present

Here are the variables affecting the effect:

* Emergency versus non-emergency situations
* Ambiguity and consequences
* Understanding of environment
* Priming the bystander effect
* Cohesiveness and group membership
* Cultural differences
* Diffusion of responsibility

Of those, I only see that only diffusion of responsibility is actually involve the present of other people. The rest seems to be independent with it. So why is the effect is stated as above? Is it possible to have this effect in a 1-to-1 situation?

Related: Is the lack of eagerness to contribute to the group's goal a cause for diffustion of responsibility?

# Answer
> 1 votes
"Bystander effect" means that if you measure the probability that someone will help a victim, you find a lower probability if there are other people present than if they are alone. The only time it makes sense to speak of a "bystander effect" is by testing that contrast: intervention probability alone vs. intervention probability with others present.

However, the Wikipedia page is not only talking about this specific "bystander effect", but also mixing in a broader collection of studies that measure *probability of a bystander intervening*. The header is "variables affecting bystanders"; the effect called "bystander effect" would be the specific case where the "variable affecting bystanders" is "presence of other people", but for a broader perspective the Wikipedia article is talking about other variables. For example, in one of the studies referenced:

> Faul, M., Aikman, S. N., & Sasser, S. M. (2016). Bystander intervention prior to the arrival of emergency medical services: comparing assistance across types of medical emergencies. Prehospital Emergency Care, 20(3), 317-323.

they've fit a logistic regression model where the outcome (dependent variable) is "bystander intervention" and the predictor variables include gender, age, urbanicity, location, severity/condition (based on EMS's first impression of the case), and type of EMS response. **They are not measuring 'bystander effect', and don't intend to.** In fact, in some of the cases in their model, no bystander intervened because *there was no bystander* at all. They're looking more generally at reasons for bystander intervention/not.

I'm also not really sure where you got that phrase "depends on", as it isn't present in the Wikipedia page you link, but generally if you do encounter that phrase with respect to *bystander effect* I would take that to mean that **the *size/magnitude* of the bystander effect depends on (item)**; this is dependence in the statistical/probability theory sense, in contrast to an effect being "independent" of some characteristic. There's no need for a moderating variable to be related to the primary manipulation of a study.

For example, let's say you measure bystander effect in a psychology laboratory by putting your participant in a room with one or more actors, and one of the actors drops some books they are carrying. You calculate bystander effect by measuring the rate at which your participant helps with the books when the only people in the room are the participant and single actor, or when there are 4 other actors present who do nothing about the books. Let's say you do this with a few dozen different participants and find that on average they are *twice as likely* to help when they are alone with the book-dropper.

Now, you repeat the experiment, except your participants spend 30 minutes browsing StackOverflow before they go into the room. In this case, you find that your participants are now *three times as likely* to help when they are alone with the book dropper. You could now say *the bystander effect is dependent on browsing an internet Q&A site*. You don't mean the bystander effect is *caused by* internet Q&A, and browsing an internet Q&A site doesn't have any relationship to "number of people in the room", but you've found a statistical dependence. You should probably do some other comparisons, though, too, to help understand what's going on: for example, was there a bigger effect because fewer people responded in a group, or because more people responded when they were alone with the book dropper, or parts of both? You might generate some more experiments to discover how specific this effect is and what parameters matter - is it specific to StackOverflow or do pictures of kittens have the same effect? Do you get the same result if participants complete a math worksheet or programming exercise? Etc..

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Tags: social-psychology, motivation, diffusion-of-responsibility
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# Question
Title: Should raw response time data be transformed?
I am a statistician and doing some data analysis in cognitive sciences. I noticed that the distribution of response time (RT) is chisq-squared-like, and I want to do Box-cox transformation to make it look normal distributed. Because before I did not think much for this transform, my question is:

* Does a box-cox transformation need to be applied to response times?
* If so, what do the results mean?
* For t-test, ANOVA and other tests, will the result be valid for the original response time data?
* If not, should we transform the data since analysis of these data is based on the normality hypothesis?

# Answer
This article by Whelan (2010) is one of the best introductory papers I've found on the subject. Normalization is covered quite clearly and extensively, including the caveats and "gotchas".

### References

* Whelan, R. (2010). Effective analysis of reaction time data. The Psychological Record, 58(3), 9.
> 2 votes

# Answer
You can transform RT, i.e., by log(1/RT). This makes the distribution roughly normal. The problem is that you don't usually run the ANOVA on the RT values collected at each trial, but on the average for each participant. So the distribution across participants need to be normal. A trick is to transform the single RT values, calculate the mean for each participant and condition, and then transform the value back with the inverse.

Alternatively, you can run ANOVAs without corrections if you use the appropriate one (i.e., normality not assumed... this will lead to oddly-looking DOF with decimal values).
> 4 votes

# Answer
My impression is that, recently, a consensus began to form recently that RTs should be transformed to satisfy model assumptions. This is especially true when data is analyzed with mixed models instead of ANOVAs.

Concerning the stability of effects under different transformations, you may find this paper interesting: http://web.uvic.ca/psyc/masson/KMR10.pdf
> 2 votes

# Answer
\[ I realize that I am 7 years late, but I still think this is worth responding to in case anyone comes across this in the future\]

No. As Max Di Luca pointed out, we perform our analyses on the mean (or median) RTs, not the underlying distributions of each individual's data (unless you are doing linear-mixed effects). Furthermore, transforming them tosses away information. What if the underlying effect is due to the effect only occurring on 10% of the trials? If the effect lengthens the RTs, it will increase the mean, but by transforming the RTs (e.g. 1/RT) then you've effectively compressed the right tail, reducing the influence of those trials. But, it might be those very trials that are driving the effect in the first place!

For outliers, I use a robust method such as MAD (e.g. +/- 3 MAD sds).
> -1 votes

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Tags: statistics, reaction-time
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# Question
Title: How is 'purple' both ligt at one wavelength and the sum of light at two different wavelengths?
I see purple, violet, magenta, etc. as very similar shades and don't understand why.

Consulting color wavelength charts like we see that purple (or violet) is about 400 nm.

Consulting color mixing charts we see that purple is also the result of adding red (665 nm) and blue (470 nm) light.

I find that confusing looking at the receptive fields of human eyes. My naïve guess is that 400 nm light would trigger the S cone almost exclusively (and not that much), where as red (665 nm) and blue (470 nm) light combined would trigger S a lot and L a decent amount. These two scenarios seem quite different to me.

Is it known why these quite different stimuli result in the same sensation of 'purple'.

# Answer
This was pointed out by Newton after his investigation with prisms. A color can be the result of a single wavelength, or the combination of different lights with different wavelengths, called metameres (lights that look the same but are physically different). A solution was proposed by Young. He suggested that color metameres could be explained by a discrete number of light receptors with different wavelength sensitivity, which he accurately predicted to be threefold (therefore hypothesizing the existence of cones). Think of a single cone, like the S-cone from your graph. For a pure light at 420nm, the cone sensitivity is half its peak. If you change the wavelength of the light to 440, then the cone will essentially double its response. Now if you keep the light at 420 but double its intensity, the cone will also double its response. So you cannot perceive color based on a single cone, because based its response you couldn't tell the difference between a change in intensity (brightness) or color (chroma). For perceiving color, you need more than 1 cone, and what matters is the relative response between the cones. While the overall response tells you the how bright the object is (technically its looks like only the M and L cones contribute to brightness perception, but this is a detail). Now if you had cones with peak sensitivities randomly distributed (assuming a very large number of cones), there would never be ambiguity in what color is being presented, because you would always have a pair of cones that would have different responses. The fact that there are metameres tells you that this number of types of cones must be small. That's essentially Young's great intuition on the topic.

Later Maxwell tested this hypothesis explicitly. Think of it as a set of equations with N unknown. We know from the laws of arithmetic that you need N different equations to solve the unknown. Maxwell used that property in his *color matching experiment*. Basically he presented one color on one half of a field and built a device that allowed him to vary the intensity of 3 lights on the other half (technically one light was subtracted to the first half for experimental convenience, but the logic holds). He showed that using this device he could match any color displayed on the first half. But you cannot do that with only 2 lights. This demonstrates conclusively that there are 3 discrete types of cones in the eye. Using this technique it is even possible to build arbitrary color spaces, which is how the CIE XYZ color space was invented, even before we knew the true sensitivity function of the cones. That's the answer to your question: the only thing that matters is that the 2 lights additively stimulate cones the same way that the single pure light would. Your brain therefore cannot tell the difference, because all it "sees" is 3 numbers coming from 3 types of cones.

So metameres are sets of lights that stimulate the 3 cones with the same relative intensity. It means that what we perceive of colors is actually a very poor representation of the complexity of a light spectrum (even within the very narrow range of wavelengths we perceive). Yet it is also lucky, because it means that we can recreate any color using a combination of just 3 lights. Maxwell understood that and here again showed that he was not only the greatest theorist of his generation but also a brilliant experimentalist by taking 3 pictures of the same object behind colored filters. Then he back-projected the pictures using the same filters to demonstrate that he could recreate the color of the object. The actual demonstration didn't work very well, but the point is that he gave the key for the technology that is now in every single display on the planet: using 3 LEDS (RGB) to display colors. This is based on the aforementioned XYZ color space. If you take a picture based a filters that produce a given color matching function, you can then convert it to a display that has different filters as long as you measured the color matching function of this display. This color space (CIE XYZ) is really remarkable because even though its input is physical (intensity of a light at a given wavelength), the output is psychological (what color humans perceive). In facts this space is constructed based on an average observer. But, based on the fact that you perceive colors that seem at least broadly correct on many different displays, it works very well.

https://en.wikipedia.org/wiki/James\_Clerk\_Maxwell#Colour\_vision
> 1 votes

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Tags: perception, vision, color, sensory-perception
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# Question
Title: At what age does logical reasoning typically develop?
Mathematics appears to be almost entirely neglected in early childhood learning. As both a mathematics teacher and father home-schooling his four-year-old daughter, I am particularly focused on teaching mathematical reasoning.

Consistent with the conclusions of Ginsburg et al, my daughter had a very natural grasp of number, operations, shape, space, measurement, and pattern from the time we began (age two). Imitation and rote were clearly the more natural mechanisms of learning at that age, as they remain now. And, as was discussed in another post, mathematical logic did not appear until she was approaching four years old. Now, her logic is limited more by her ability (or otherwise) to focus, and to organise her thoughts.

A lot of data exist relating age with typical cognitive abilities, but these are necessarily influenced by our collective culture of education. *Has any rigorous research been done to determine when particular cognitive abilities can be developed, for example deductive as opposed to inductive reasoning?* For early childhood development, *can educators know what is possible or (generally/typically) impossible to teach at a certain age, or what is appropriate or inappropriate?*

Thank you.

# Answer
> 1 votes
A study (1) found that while 10% of 6-year old children used the conditional proficiently, 50% of 8-year old children not only could use it proficiently but also understood what the conditional meant. The conditional is one of the two basic verbal forms we use for expressing a logical reasoning, together with syllogisms.

It should be noted, however, that most of the time, most people don't bother articulating reasons, even when it seems that they must have reasons so say what they say.

Aristotle already discussed extensively enthymemes, i.e., implicit reasoning where part of the reasoning is clearly missing, although usually easily retrievable. The speaker may for example state one premise, leaving the audience to guess the conclusion from both the stated premise and the context of the conversation. Guessing is also usually performed intuitively, the brain somehow processing the relevant data without any conscious effort on the part of the listener.

Given this, it is debatable whether reasoning starts with verbal communication. It may come before language. However, if you define reasoning as verbally articulating reasons, then reasoning starts at least potentially around 6-8 years of age in a majority of children.

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(1) Julia R. Badger, University of Oxford, and Jane Mellanby, University of Oxford, Producing and understanding conditionals: When does it happen and why does it matter? -- Journal of Child Language Acquisition and Development, Vol 6, Issue 1 21-41 (March 2018)

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Tags: learning, educational-psychology, mathematical-ability, children
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# Question
Title: Transforming Response-Time Data for normal distribution?
I am a psychology student and currently working on my master thesis. I have developed an experimental paradigm (Dot-Probe Paradigm) in which participants have to react to words, that are presented on their screen.

I have different trial types of words:

misophonic (e.g. smacking) - neutral (congruent: Dot appears on the side of the misophonic stimulus)

misophonic - neutral (incongruent: Dot appears on the side of the neutral stimulus)

negative - neutral (congruent)

negative - neutral (incongruent)

neutral - neutral (Baseline)

In order to test, if all participants have the tendency to react quicker to negative words, I calculated the means of the trials:

negative - neutral congruent and negative - neutral - incongruent

Then I subtracted them:

Attentional Bias(neg): (Mean: negative - neutral - inkongruent) - (Mean: negative - neutral congruent)

Now I would like to do a one-sample t-test, but my Attentional Bias (neg) is not normally distributed.

I have read that I could do a log-transformation of my variable but I am not sure if I have to log transform my raw data, the means or the calculated AttentionalBias(neg) component.

So my question is: At what step of my analysis do I have to log-transform my data?

Any advice would be very much appreciated!

# Answer
First, it's your *residuals* that need to be normal, not your data. https://stats.stackexchange.com/search?q=normal+residuals

For example, if you are doing a two-sample t-test and your data are bimodally distributed, that could very well be just because your two groups have different means. For regression problems with more parameters, you may see a very non-normal distribution in the data but yet the residuals are perfectly normal once you account for all your predicting variables.

You're right, though, that reaction times are typically not normally distributed. I would log transform the original values. Once you've log-transformed the data, the meaning of all of your comparisons changes. Namely, subtractions on the log scale are equivalent to *ratios*. This works well for time intervals, because it changes your interpretation from "group A is XX seconds longer than group B" to "group A is XX times longer than group B". This contains an inherent normalization for the length of A.

Generally, I would favor some form of ANOVA rather than reducing your problem to a one-sample t-test on a subtraction; there are a lot of problems in data that you can catch this way that you wouldn't notice with the one-sample test. Once you've subtracted, it's less clear where the actual differences are across the different dimensions of your data.
> 1 votes

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Tags: reaction-time
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title: Question regarding inferiority complex

text:
# Question
Title: Question regarding inferiority complex
> "***The more one has feelings of inferiority, the more one has a power attitude, and the more one has a power attitude, the more one has feelings of inferiority***"

This above paragraph was said by Carl Gustav Jung.

I observed that some people try to show that they are more powerful and always wants attention in group of people and for that purpose they humiliate others and make them feel incomplete means they knowingly & unknowingly makes other person also inferior.

**Question 01** : Is such things are the symptoms of ***inferiority complex***?

Because they feel inferiority in their minds so there may be possibility that want to remove their inferiority in their mind by showing their power.

**Question 02** : How to deal with such people and what are the cure of such complex?

# Answer
> 1 votes
"Inferiority complex" is an old idea from non-scientific study of psychology.

If you look for recent papers, you'll find that most are either in very low-quality journals, occur as literary or similar analyses rather than real human psychology, or are puns/jokes/references to the concept rather than actually about "inferiority complex" in psychology. For example, this one:

> Assimon, M. M., Cutter, G. R., & Bargman, J. M. (2022). The Non-Inferiority Complex: What Do Non-Inferiority Trials Tell Us?. Journal of the American Society of Nephrology, 33(4), 674-676.

A non-inferiority trial is a type of statistical design where instead of testing a null hypothesis that two treatments are not different and declaring a statistically significant result when you observe a difference larger than expected by the null hypothesis, you test a null hypothesis that two treatments are different by at least some margin, and declare a statistically significant result when you observe a difference smaller or in the other direction as expected by chance if the null hypothesis is true. This has nothing to do with "inferiority complex" in psychology, of course, but the author gave the paper a cute name making reference to the old-fashioned idea.

The idea of the inferiority complex goes back to Alfred Adler, a contemporary of Freud. Reading about Jung, Freud, and other similar past figures in the field might be useful to understanding the *history* of psychology, but just like we don't use Galen or Aristotle in treating modern medical patients, I'd highly recommend against using Jung or Freud to understand actual psychology.

> I observed that some people try to show that they are more powerful and always wants attention in group of people and for that purpose they humiliate others and make them feel incomplete means they knowingly & unknowingly makes other person also inferior.

It sounds like you are describing bullying behavior. There are lots of explanations for bullying, but generally the attempts to scientifically link perpetration of bullying to low-self esteem are mixed or show very modest associations, for example:

Tsaousis, I. (2016). The relationship of self-esteem to bullying perpetration and peer victimization among schoolchildren and adolescents: A meta-analytic review. Aggression and violent behavior, 31, 186-199.

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Tags: social-psychology, personality, behavior, jung
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# Question
Title: Looking for literature on detailed developmental milestones (and their prerequisites) for a child of a given age
I would like to know if there is any scientific literature on the detailed developmental milestones in different domains(cognitive, language etc.,) that a child of a given age is supposed to reach.

A couple of e.g.,

1. The child does not feel the need to resist/communicate when a unknown person takes his belongings before him. I would like to understand the reason behind this, it could be that he does not have a sense of ownership over his belongings, or he is not paying enough attention to what is happening around him or it could be that he does not know how to react to that situation.
2. The child does not give correct answers to questions on what happened in the past e.g., what did you eat for breakfast? The reason could be that he does not understand the question, or he is not able to recollect what he was eating may be because he was not paying enough attention or his abstract thinking ability is not mature enough.

The reasons that I discussed for the above observations are purely based on my understanding of his condition(and therefore could be wrong) and not based on any scientific evidence. I would like to know if there is literature which could throw light on each such small milestone(for lack of a better word) that a child of a given age is supposed to reach and the prerequisites understanding he should have for reaching there. These subtle behaviors are usually not mentioned in milestone charts available with a pediatrician.

# Answer
> 3 votes
A good resource for psychological development is:

Sigelman, C. K., & Rider, E. A. (2017). *Life-span human development 9th Edition*. Wadsworth Publishing.

A sample can be viewed at https://read.amazon.co.uk/sample/B0B4HM74RH?f=1&l=en\_GB&r=9c594c00&rid=BYKJA17MSRREJFXQKE88&sid=258-8304090-2678614&ref\_=litb\_m

## A point of note

As mentioned in the comments, if you want to study the milestones in detail like that you will need to bear in mind the fact that every psychologically healthy child can develop at different rates, and so the milestones cannot be followed rigidly. They serve as a guideline only.

The whole literature needs to be borne in mind, as the developmental theories behind the milestones do have their critics, and the development of these developmental theories will need to be fully understood.

My answer to a question on development at https://psychology.stackexchange.com/a/17211/7604 will give you a small glimpse into what I am talking about here.

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Tags: developmental-psychology, language, autism, language-processing, cognitive-development
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# Question
Title: Is meaning-seeking behavior a biological optimization problem?
In short, I'm interested in cognitive, neuroscientific, biological and/or computational perspectives on what we vaguely refer to as meaning seeking. Of course, this is a large topic, but any information would be highly appreciated.

## Background

Humans tend to desire meaning in their lives. While it would be hard to agree on a precise definition of *meaning*, it often refers to positioning oneself in a way that is compatible with one's beliefs, ambitions and values, allowing the individual to make sense of the world and of himself, and to pursue whatever (often transcendental) goals he considers worthy (i.e. meaningful). In simpler words, meaning could refer to making peace with the perceived reality of the world and with oneself. At first glance, it seems to me that a meaningful existence requires **the absence of cognitive dissonances**, but I wonder what science would have to say about this, and if there is any empirical basis for claiming this. Or perhaps the questions is misformulated and such behavior should not be put into the domain of meaning?

## Possible explanations

A simple evolutionary argument could be that meaning-seeking behavior originates from our impulse to belong (isolation means death), but how do we then explain hermits or dissidents or all other individuals who have effectively made themselves suffer/die in order to uphold meaning in their lives (i.e. dying for one's beliefs)? So the argument that meaning-seeking behavior is a purely evolutionary phenomenon that serves only to maximize one's potential for reproduction doesn't appear sufficient.

## Questions

1. Can meaning seeking be thought of as an **optimization problem of some biological parameters** on an individual level, e.g. in terms of energy required for various cellular processes, homeostatic gene expression dynamics etc.? For example, depression (which can have an existential origin) is damaging to health and has been linked to epigenetic modifications (Sun et al. 2012), so having a mechanism that would seek to minimize such damage would seem to be beneficial for an organism.
2. Can we construct a more formal definition of meaning that would be less anthropocentric? In other words, how far would we need to curb the definition so that humans would no longer qualify as the only meaning-seeking organisms? Or are we indeed the only species with the required neural capacity to express such behavior?
3. Could modern experimental methods such as EEG, fMRI, gene expression profiling and epigenome sequencing be used to answer some of these questions at least to a degree? E.g. would a comparison of individuals who claim to live a meaningful life vs those who don't make any sense? Of course, even if a some significant differences were observed, an obvious next question would be what caused them, i.e. a mind-body-environment problem ...

I'd be happy to know at least if there are some research groups or labs that try to tackle such questions.

# Answer
> 4 votes
> it seems to me that a meaningful existence requires the absence of cognitive dissonances, but I wonder what science would have to say about this, and if there is any empirical basis for claiming this.

The difficulty, as you've pointed out, is that there isn't agreement on the definition of "meaning" in this context. Meaning can be interpreted by different people (and cultures) variously as: "accomplishment", "social good", "altruism", "realizing potential", "inner peace", "knowledge", and on and on.

> the argument that meaning-seeking behavior is a purely evolutionary phenomenon that serves only to maximize one's potential for reproduction doesn't appear sufficient.

Read about evolutionary explanations for altruistic behaviour for example to see how this can be addressed: "Every single instance of altruistic behavior need not always increase inclusive fitness; ... it would be beneficial to err on the side of caution and usually be altruistic even if in most cases there were no benefits."

> how far would we need to curb the definition so that humans would no longer qualify as the only meaning-seeking organisms?

"Social good" and "altruism" are examples of meaning-seeking behaviours commonly found in many animal species.

> Could modern experimental methods such as EEG, fMRI, gene expression profiling and epigenome sequencing be used to answer some of these questions at least to a degree?

Sure, why not. For example: "Altruism, the experiment suggested, was not a superior moral faculty that suppresses basic selfish urges but rather was basic to the brain, hard-wired and pleasurable."

> I'd be happy to know at least if there are some research groups or labs that try to tackle such questions.

The area of psychology most likely to address such an abstract concept as meaning-seeking is probably Humanistic Psychology: "Human beings are intentional, aim at goals, are aware that they cause future events, and seek meaning, value, and creativity."

You can read about research done in this field \- there isn't very much of it though - and also about self-actualization (another common interpretation of meaning-seeking in psychology).

# Answer
> 1 votes
According to Applied system-vector psychoanalysis meaning-seeking behaviour is a side effect of the evolutionary formation of the purported "audial vector".

"Audial vector" is a characteristic of increased audial sensitivity of primeval tribe members who carried out the function of night guards of the tribe. Given that function, they had ample time to spend in solitude and meditate over all sorts of matters, including abstract questions such as the meaning of life.)

(Important disclaimer to make is that this Neo-Freudian/evolutionary psychology concept, albeit intriguing, does not present any empirical evidence of its claims.)

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Tags: cognitive-psychology, neuroscience, cognitive-neuroscience, philosophy-of-mind, theory-of-mind
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title: What is a sweet pain, exactly?

text:
# Question
Title: What is a sweet pain, exactly?
Why some pains are sweet? Some pains give pleasure not even bodily pains but mentally also in daily affairs, an individual may intentionally impose mild difficulties on his self. Is there a cognitive or evolutionary reason behind it or it is a disorder?

# Answer
Endorphins and flow experience I suppose. Seems adaptive enough to have some mechanism for overcoming short-term distress for the sake of long-term gains, but like most things, this can be taken to extremes. There's some debate regarding the status of masochism within the normal–abnormal spectrum. See also internalization, which includes self-harm among other forms of maladaptation.
> 2 votes

# Answer
According to Applied system-vector psychoanalysis masochism happens among people with dominant "dermal vector" who have been endured painful physical punishments in childhood.
> 0 votes

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Tags: cognitive-psychology, sensation
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# Question
Title: What does it mean if a neuron is "expressing" something?
Sorry for the simple question, not a neuroscientist just trying to understand a paper for school. In a study with mice, there was 2-photon calcium imaging done, and part of it read:

> We used single- and multi-plane imaging approaches to record the activity of populations of excitatory neurons and two inhibitory classes, Somatostatin (Sst) and Vasoactive Intestinal Peptide (Vip) expressing interneurons, across multiple cortical depths and two visual areas (VSIp and VISl)

First I thought this meant that SST & VIP were inhibitory neurons. But when I Google it says they're hormones.

So is this saying they recorded activity from inhibitory interneurons that were ... releasing? producing? ... SST & VIP ? What does "expressing" mean in this sense.

# Answer
## Gene Expression

"Expressing" refers to gene expression \- in biology we say a cell is "expressing" a gene when the products of that gene are present. "Sst-expressing cell" is a way of saying "cell that has somatostatin protein present", or at least "has mRNA present for producing somatostatin protein" - biologists are not always explicit about whether they mean they measure mRNA or protein when they talk of expression, and in modern days often a "Sst-expressing cell" is identified by producing some reporter protein like green fluorescent protein (GFP) under a somatostatin promoter (or, most likely, dependent on a strain of mouse that uses Cre-recombinase to only produce GFP in cells where Cre is produced under a Sst promoter).

## Classifying Interneurons

There are lots of different interneurons; they are difficult to classify. Here are a couple papers to read:

Markram, H., Toledo-Rodriguez, M., Wang, Y., Gupta, A., Silberberg, G., & Wu, C. (2004). Interneurons of the neocortical inhibitory system. Nature reviews neuroscience, 5(10), 793-807.

DeFelipe, J., López-Cruz, P. L., Benavides-Piccione, R., Bielza, C., Larrañaga, P., Anderson, S., ... & Ascoli, G. A. (2013). New insights into the classification and nomenclature of cortical GABAergic interneurons. Nature Reviews Neuroscience, 14(3), 202-216.

One way to classify some of these interneurons is by their expression of particular genes. Using that scheme, it then becomes common for, say, "Parvalbumin-expressing cells" (=cells that have parvalbumin protein/mRNA) to get shortened into just "Parvalbumin cells" or "Parvalbumin interneurons" or "PV+ cells", etc.

It's not necessary that these proteins that are used to name cell types are particularly crucial to their function; for PV cells, it seems like it is, because one feature of PV cells is that they have very fast electrophysiological kinetics, and some of those fast kinetics are assisted by the calcium binding of parvalbumin. For somatostatin interneurons, it's less clear; somatostatin is certainly an important gut hormone, but it's not particularly clear why somatostatin-expressing neurons form a particular important subclass of cells in the brain, as most known functions of somatostatin are restricted to development or the gut.

## Back to the Question

> So is this saying they recorded activity from inhibitory interneurons that were ... releasing? producing? ... SST & VIP ? What does "expressing" mean in this sense.

They're saying they recorded activity from inhibitory interneurons that have been grouped in the past according to their production of SST and VIP mRNA or protein. They aren't necessarily interested in either SST protein or VIP protein, but these have served as markers/names for particular cell populations. The primary neurotransmitter that brain SST and VIP interneurons produce is neither somatostatin nor vasoactive intestinal peptide; the primary neurotransmitter for both is GABA. You'd be able to find out a lot more about those cell populations by reading other papers containing terms like "Sst interneuron" or "VIP interneuron".
> 3 votes

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Tags: neuroscience, neurophysiology, brain, neuroimaging
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