# Question
Title: What is the difference between noise reduction and noise cancellation?
I had a question about sirens in another section which led to a question in physics section...and I was told my question is more suitable for cognitive science. So here it goes:

There are many kinds of noises: from a heavy truck going by to the wailing of sirens from an ambulance. Then there is someone next to you snoring. Although they are all bothersome, they can't be the exact same thing?

I've heard people use the term "white noise" to cancel out or reduce other noise. Granted I have used various earplugs (which reduce only reduce certain kinds of noise and not that well either), but looking at white noise, I realized there is so much about noise and sounds that I don't know about. For instance there is also brown noise and pink noise. There is a sound's loudness, pitch, timber, direction, frequency, etc.

How do I go about finding the right kind of sound masking for different kinds of sounds like snoring and wailing ambulances?

# Answer
Let's start with the terminologies in your question:

**Loudness**: The level (amplitude) of the sound. The higher the sound level, the louder it is perceived. Loudness is measured on a dB scale, *e.g.* dBA (corrected for the human sensitivity across frequencies), dB HL (used in the clinic relative to normal-hearing level) or dB SPL (a more physical approach to sound level). In Figure 1 below an impression is given in dBA (A-weighted sound levels). Don't worry about dB scalings too much. Generally spoken, normal speech is around 65 dB, background noise around 30 dB and the pain threshold around 130 dB (source: OSHA).

Fig. 1. Sound level chart. source: IQ

**Frequency**: A perfect sine wave has a single frequency. This corresponds to a pure tone. Most normally occurring sounds have multiple frequencies. Frequency determines pitch.

**Pitch**: Basically determined by the frequency of the sound. The audible frequency range of humans ranges from approximately 20 Hz to 20 kHz (source: LSU). The subjective perception of frequency is called pitch.

*Timber*: no, no, timber has something to do with wood - it's **timbre**. Timbre represents 'those subjective qualities of \[sounds\] not determined by \[their\] pitch our loudness. It is determined by the frequency spectrum and envelope (envelope is the slow, low-frequency part of the sound that envelopes it) (source: wiki). In terms of sound attenuation/masking/cancellation, it is of not much interest. Likely the timbre can influence the nuisance factor of a sound, but not more.

**Direction**: acoustically generally defined as azimuth (degrees in horizontal plane) and elevation (degrees in the vertical plane). Also here, in terms of sound attenuation/masking/cancellation, it is of not much interest

**White noise**: A random signal with a constant power spectral density. It is a discrete signal whose samples are regarded as a sequence of serially uncorrelated random variables with zero mean and finite variance. One may also require that the samples be independent and have the same probability distribution. If each sample has a normal distribution with zero mean, the signal is said to be Gaussian white noise (source: wiki). **Subjectively, white noise has a sharp, rather unpleasant hissing quality to it.** Check it out at Online Tone Generator.

**Pink noise**: Pink noise or 1⁄f noise is a signal or process with a frequency spectrum such that the power spectral density \[...\] is inversely proportional to the frequency of the signal. \[E\]ach octave \[...\] carries an equal amount of noise energy. The name arises from the pink appearance of visible light with this power spectrum (source: wiki). **Pink noise has much higher low-frequency contribution than white noise, and is therefore more pleasant to the ear. It approaches the sound of rainfall, or that of a waterfall. Pink noise is a better choice when you wish to go to sleep, as it is often experienced as relaxing**. Check it out at Online Tone Generator

Brown noise doesn't exist, as far as I know. **Brownian noise** is what you are after. Brownian noise, or red noise, is the kind of signal noise produced by Brownian motion, hence its alternative name of random walk noise. The term "Brownian noise" comes not from the color, but after Robert Brown, the discoverer of Brownian motion. The term "red noise" comes from the "white noise"/"white light" analogy; red noise is strong in longer wavelengths, similar to the red end of the visible spectrum (source: wiki). It is a much less commonly encountered noise. Check it out at Online Tone Generator

On to your question:

There's basically three things you can do to get rid of pesky sounds:

1. **Attenuation**. This is a typically a **passive** way of noise reduction, which can be accomplished by blocking the noise with ear plugs, ear muffs, sound-proof walls etc. Ear plugs come in a huge variety, ranging from a couple of foam ear plugs for a few cents per pair to sophisticated ear plugs of hundreds of bucks, to the hand-made, individually tailored plugs available from medical professionals. The latter, obviously, are the best. They are used by professional musicians for example and are made by professionals by making a cast of your outer ear and molding a perfectly fitting shape into it. All these plugs do, however, is dampen the sounds, *i.e.*, lower the sound level. The better ones attenuate sounds with a good many dBs (say 30 to 40 dB) with a 'flat frequency characteristic', meaning they attenuate all audible frequencies in roughly the same way. The cheaper ones attenuate poorly, and worse, often their frequency characteristics show a peak at the higher frequencies and low performance at the low frequencies. This causes bass noises to come straight through (snoring, musical drums etc.). However, even with a rockstar plug of -40dB, you will reduce a siren passing close by with only 40 dB, leaving about 70 dB (depending on the distance from the siren of course).
2. **Masking**. This is an **active** approach, where you don't attenuate the background noise, but you mask it with a more pleasant sound. White noise is ideal, as it encompasses all audible frequencies. This means that whatever the noise source is, it will be effectively masked by the white noise. The pink noise may, however, be a better candidate, because it is more pleasant to the ear than white noise, as said. At the higher frequencies, pink noise will perform less well than white noise, however, so the ambulance wail will come through relatively loud. Low-frequency noises like snoring are masked well. In fact, pink noise is often used for babies and adults to sleep, because it is a rather pleasant sound. However, to mask a sound with a certain frequency spectrum of 70 dB, you need an equal 'amount' of pink noise in the same frequency band to mask it completely. Since low frequencies are well represented in pink noise, low-frequency sounds of relatively low sound level are masked pretty well, such as snoring, or the pesky bass of the neighbors TV. To block out a siren, or the noise of a full blown house party, you should turn up the pink noise so loud that it simply wouldn't do you any good.
3. **Cancellation**. This is intelligent **active** sound masking, also called active noise. Here, a device records the surrounding noise with a microphone and a built-in speaker generates sounds reversed in phase with the same amplitude. Theoretically, this perfectly cancels out the noise, whatever the frequency, whatever the level. Protection of a "1-dimension zone" is relatively straightforward and requires only one or two microphones and speakers to be effective. Several commercial applications have been successful, especially the noise-cancelling headphones. The term "1-dimension" refers to a simple pistonic relationship between the noise and the active speaker (mechanical noise reduction) or between the active speaker and the listener (headphones). Cancellation of sounds in a 3D environment becomes challenging (source: wiki).
> 7 votes

# Answer
I'm not sure but you what you might want to learn is phase cancellation. Sound is a wave, the compression and dilatation of the air between the source of noise and your ears. If you add another sound, where the waves are exactly the opposite of the first one, they will both disappear. Some headphones use this technique to reduce the sound. They detect the sound around you and cancel it by creating an opposite sound.

https://en.wikipedia.org/wiki/Active\_noise\_control

Edit : Actually you can see more illustrations here :

https://en.wikipedia.org/wiki/Sound

Two dimensional diagram are usually used to represent the vibration. Your ear doesn't hear all the sounds. You can add several sounds together. They will be mixed and this will change the way you hear it.
> 2 votes

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Tags: hearing, psychoacoustics
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# Question
Title: Voltage sensitive dyes technique: 2-photons microscopy vs confocal microscopy
I just discovered voltage sensitive dyes technique and I was wondering what would be the advantage to use 2-photons microscopy compared to confocal microscopy?

They are both fluorescent techniques which can measure photon's emission, in most of the cases it looks like 2-photons microscopy is preferred over confocal microscopy, but why is that?

# Answer
Confocal Fluorescence Microscopy and 2-photon Fluorescence Microscopy are two techniques commonly used in neuroscience to image only one plane of the sample and thus increase resolution. However, how they achieve this technically is distinct.

**Confocal (confocal laser scanning microscopy (CLSM))** In confocal microscopy the sample is scanned with a laser in X and Y coordinates and fluorescence is recovered by de-scanning the emitted photons. To select photons emitted only in the imaging plane (focal plane), a pin-hole restricts the collection of the emitted light allowing only the passage of photons emitted in the plane one is currently imaging.

*This image exemplifies how emitted photons (dashed red beam) originating outside of the focal plane will be blocked by the pinhole before reaching the detector.*

This has several consequences

1) The laser light **will** excite fluorophore which you are not imaging (because the emitted photons are blocked by the pinhole). This bleaches your sample below and above your imaging plane while you are not collecting information from those planes.

2) The emission path has to be de-scanned in order for the pinhole to work. This long path from the emission to the detection of the emission photons means that you are loosing some precious emission photos.

**2-photon Scanning Laser Microscopy**

In the case of confocal microscopy excitation is achieved by the acceptance of 1 high energy photon. However, in 2-photon microscopy, two photons of half the energy are used to excite the fluorophore.

This introduces a non-linearity that has the following immediate consequence : if you need to 2-photons to coincide on the same fluorophore to excite it then you will only excite molecules of flurophore in a small volume of space in which the intensity of the laser is sufficient. Then since the excitation of molecules is limited to a small volume in x,y,z.

*This image shows the difference between excitation when done with single photon (left) and 2-photon (right). Black is the areas where the excitation took place. As you can see on the left the single photon excitation excites planes below and above the imaging plane.*

Then 3 things happen

1) You can restrict your imaging to a plane without the need of adding a pinhole. In Confocal the pinhole restricts the passage of photons emitted from planes other than the imaging plane. In 2-photon your effective excitation is already restricted in the Z plane, so the emission will also be restricted to this plane.

2) Since you now don't need a pinhole, you don't need to de-scan the emission. This means you can put your detector (Photon Multiplier Tube: PMT) very close to where the emission happens. Now you want all the photons you can get, because they all come from your image plane!

3) You are not bleaching other Z planes of your sample, because the intensity in other planes is not enough so that 2 photons excite the fluorophores.
> 6 votes

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Tags: neuroscience, electrophysiology
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# Question
Title: Why cerebellar input fibers use 2 ways to send a siganl to DCN?
Both groups of input fibers of cerebellum (mossy, climbing) start 2 pathways: 1) project directly to the deep nuclei 2) project to cerebellar cortex, which then (after some processing) sends projection back to deep nuclei through Purkinje cells.

What is the purpose of such an architecture?

And closely related question: is the input information to DCN (the first pathway) and to cerebellar cortex (the second pathway) the same?

# Answer
**Short answers:**

1) The true purpose of this architecture is not known (yet).

2) Yes, it is the same information, since the signal comes from the same axon (for climbing fibers see e.g. De Zeeuw et al., 1997).

**Comment on the first answer:**

Of course, though, there are many theories about the function of the cerebellar circuits, including these collaterals of the mossy and the climbing fibers. I would refer to the articles on wikipedia and scholarpedia as entry points.

To give you an **extremely simplified** scenario where such an architecture could be useful:

Let's say the mossy fibers contain the motor plan, coming from the cerebral cortex and the climbing fibers contain the true state of the limbs coming from the peripheral sensors (formulated like this, these statements are certainly not true). Now the direct signals to the deep cerebellar nuclei (DCN) could be used to quickly compute a rough "movement error" (i.e. planned trajectory vs. real trajectory) that already initiates a quick, rough movement correction. The signals to the cerebellar cortex would be used to compute an exact "movement error" which is also integrated at the DCN "a bit later" (i.e. some synaptic transmissions later) to further refine the movement correction.

Again, this is certainly not what is going on in the cerebellum but might give you some intuition of why such a circuitry could exist.

**References**

* De Zeeuw CI, Van Alphen AM, Hawkins RK, Ruigrok TJ. Climbing fibre collaterals contact neurons in the cerebellar nuclei that provide a GABAergic feedback to the inferior olive. Neuroscience. 1997 Oct; 80(4):981-6.
> 1 votes

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Tags: neuroscience, cognitive-neuroscience, theoretical-neuroscience
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# Question
Title: What is the purpose of dead end neurons in this diagram?
I was reading over some sources about ANNs, and here I found this diagram of a Recurrent Neural Network (RNN, the source calls it a feedback neural network).

I noticed that a few neurons in this diagram lead to other neurons that are dead ends (have no connections to other neurons). For example, neuron *U5* leads to no other neurons, and *U9* has a connection to *U4*, but *U4* doesn't have a connection to any other neurons.

Is there a purpose for *U5* and *U4* to even exist?

Or am I missing something bigger here?

# Answer
> 3 votes
As said in the comments, $U\_4$ and $U\_5$ are not used to compute the values of the output neurons.

However, in some cases one may allow the connections between neurons to change over time, in which case $U\_4$ and $U\_5$ may be later used to compute the values of the output neurons. Seanny123 gives biology as an example. For another example, you may want to look at the literature on neuro-evolution, i.e. optimization of neural architectures with evolutionary algorithms, which may allow changing the connections between neurons over generations (e.g. that's what I did for my master thesis: *Franck Dernoncourt. "The medial Reticular Formation: a neural substrate for action selection? An evaluation via evolutionary computation.". Master's Thesis. École Normale Supérieure Ulm. 2011.*, though I may have coded the mutation and crossover operators in such a way that dead-end neurons don't appear, I don't recall).

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Tags: neural-network
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# Question
Title: Is there a developmental purpose to adolescent transgressions?
Many adolescents transgress rules and break laws, not out of criminal intent or because they have some disorder, but "for fun", as an adventure, for the experience.

How is this explained from the perspective of psychology and cognitive sciences? Does this behavior serve a developmental purpose, or is it merely a dangerous side effect that is best suppressed and controlled by parents and authorities?

---

The following functions have been suggested1 for adolescent risk-taking behavior, such as psychoactive substance use, risky driving, or antisocial behavior:

* self-affirmation and experimentation / exploration
* identification and social acceptance
* ritual and emulation
* social visibility and desirability
* self-exoneration
* escape through action and excitement

But the term "risk" implies that these behaviors are not necessarily functional in the sense that they help the individual develop healthily. Smoking may lead to peer acceptance, but it is certainly not healthy.

Yet, the ubiquity of these behaviors suggests that they must serve some functional purpose. What is it?

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1 Bonino, S., Cattelino, E., Ciairano, S., Mc Donald, L., & Jessor, R. (2005). *Adolescents and Risk: Behavior, Functions, and Protective Factors*. New York: Springer.

# Answer
> 1 votes
The function of rebellion is to challenge conclusions reached by previous generations.

If the conclusions of each generation were not challenged, errors in judgment would be perpetuated, leading to larger and larger errors in subsequent generations as each successive generation built upon the false conclusions of the previous generations.

This can be observed in technological and entrepreneurial "disruptions", in which rebels (entrepreneurs) gain competitive advantages by challenging established assumptions about the market, or "conventional wisdom," and generate creative solutions that serve as more than just clones of established business models. (PayPal, Facebook, Google, Twitter, Amazon, Uber, and perhaps even Tesla could be said to have profited from this disruptive, creative paradigm.)

Adolescents transgress for many reasons, but important to remember is that they often do so not in directed pursuit of goals, but rather to explore the possibility space and establish their sense of self-determination. Later, as goal-attainment becomes important, individuals who have explored larger spaces have larger bodies of experience upon which to draw, from which they can generate creative solutions.

I have no academic sources for these assertions. They are simply observations of learning patterns that I have seen others exploit, and thus learned to exploit myself.

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Tags: developmental-psychology
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# Question
Title: Why is the initial first-line response to a psychological problem not a brain scan?
I get the impression most people having a cognitive problem are encouraged to see either a psychologists or psychiatrists (the actual medical doctors) to engage in verbal or pharmaceutical therapy. I actually knew someone who, in the '80s, was having visual hallucinations for months and seeing a therapist before she actually got a brain scan and discovered it was a benign tumor.

While I can understand that scans cost money, since repeated therapy sessions also cost money, I don't really understand why the prevailing advice isn't "scan the person's brain first, and check their blood, then try chatting with them if it isn't obvious after that". Wouldn't you want to go with the obvious, empirical objective measures first, and switch to heuristics after that?

Which isn't to say that it isn't important to have an initial conversation with the person- for the same reason a person should have a conversation with their GP- but it seems like that only makes sense as a precursor or supplement to the physical testing that also needs to happen.

# Answer
> 6 votes
The first stop when a non-emergency medical issue evolves is, as you say, a visit to the GP. This is *not* a supplement to diagnosis. Instead, a visit to the GP can be a critical step in the treatment process and a GP will assess what the **most probable** underlying cause is during a consultation, based on a physical examination and verbal communications. Then the GP can refer the patient to the proper next medical practitioner for specialized help. Note that a diagnosis involves mainly ***excluding other causes and narrowing down the list of options***.

Your case report lacks some critical information (*e.g.*, age at diagnosis *etc*.), but the statistics behind the diagnosis can still tell a lot about the GPs decision:

* The incidence of brain tumors is about 22 cases per 100,000 individuals (**0.02%**). Brain tumors are most likely to arise in kids or late teens. Dependent on the age of your friend at the time of diagnosis, this may have placed them out of that age window.
* The incidence of visual hallucinations is about 17 per 1000 **(1.7%)** (Tien, 1991), *i.e.*, orders of magnitude higher than brain tumors. In other words, just a minor fraction of visual hallucinations are caused by brain tumors. A more likely cause for hallucinations are positive psychotic symptoms, the realm of psychotherapists and psychiatrists. Most visual hallucinations are caused by psychosis (*e.g.*, schizophrenia), Parkinson's disease and Alzheimer's disease (source: WebMD). The latter two are typical cheriatric diseases (diseases linked to old age). If your friend was not considered an elderly at the time of diagnosis, it would make psychosis the most likely candidate cause of the symptoms.

Brain scans do not diagnose Alzheimer's or Parkinson's, nor psychosis. A brain scan would only, perhaps, find a tumor that has a very small chance of occurring. Moreover, a single scan may not be enough. The tumor may be small and clinical tests, fMRI, PET, or bone scans may be necessary (source: JHMI), which can result in an extensive list of scans, many hospital visits, and associated financial burden. The GP chose the best hit, and that's a psychiatric issue.

<sub>**Reference**
**-** Tien, *Soc Psychiatry Psychiatr Epidemiol* (1991); **26**(6):287-92</sub>

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Tags: abnormal-psychology, clinical-psychology, diagnosis
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# Question
Title: Is the Rubin Vase illusion an example of inattentional blindness?
Generally, people looking at an example of a Rubin Vase see either the vase, or the faces. The brain seems to make a decision on which one is being viewed, but both cannot be focused-on at the same time.

Is the Rubin vase a form of inattentional blindness, caused by the same brain function that only allows us to focus on certain objects in our field-of-view, but not others? The Gorilla-in-the-Room is another example.

# Answer
**Short answer**
The Rubin Vase is a visual illusion, which can be traced down to the way the visual system analyzes visual scenes in terms of objects and background. Inattentional blindness is not an illusion, it is the failure to detect stimuli when the mind is focused on something else. It has to do with the limitations in the capacity of the visual system to extract relevant information from a visual scene.
**Background**

* The Rubin Vase illusion (Fig. 1) is an example of an **ambiguous figure/ground illusion**. The visual system interprets patterns in terms of external objects. To do this, the visual system distinguishes objects (figure) from background (ground). In the Rubin Vase illusion, when the faces are considered background, you will see the vase as figure, and *vice versa*.

Fig. 1. Rubin vase illusion. source: TU Dresden

The visual system represents objects primarily in terms of their contours. Also, elements that are close together, or share certain features, or are homogeneous in certain respects tend to be grouped together (grouping). The sudden reversal one may perceive is thought to be due to a shift of attention on the shape of the contour. The observer's "perceptual set" and individual interests can also bias the situation. Biasing the shapes or contours can make one interpretation stronger than the other one. This particular illusion involves higher cortical processing, because previously stored information about vases and faces are resourced (source: TU Dresden).

* The Invisible Gorilla (see a video clip here) (Fig. 2) is the effect where people instructed to focus on a particular target are prone to miss other salient, sometimes striking stimuli. The classic, familiar example being subjects shown a basketball game and they are instructed to keep count of how many times the ball is passed between players in the black team. When the subjects watch the video clip and attentively count the number of passes, about half of the subjects totally miss the scene in the video where a man in a giant gorilla suit walks slowly into the middle of the screen, beats his chest and then wanders off, because they were so focused on counting the passes (that’s not to mention the other deliberate mistakes in the video) (source: Life in the Fast Lane). A newer version hits home even harder; 24 experienced radiologists were asked to perform a familiar lung-nodule detection task. A gorilla, 48 times the size of the average nodule, was inserted in the last case that was presented. Eighty-three percent of the radiologists did not see the gorilla. Eye tracking revealed that the majority of those who missed the gorilla looked directly at its location. Thus, even expert searchers, operating in their domain of expertise, are vulnerable to inattentional blindness (Drew *et al*.,, 2013).

Fig. 2. Invisible Gorilla. source: Persuasion Blog

The Invisible Gorilla is an example of inattentional blindness. Inattentional blindness can be defined as:

> **The failure to notice unexpected objects or events when attention is focused elsewhere** \[...\] (source: Simons).

**Reference**
**-** Drew *et al*., *Psychological Science* (2013); **24**(9): 1848–53
> 3 votes

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Tags: cognitive-psychology, neuroscience, perception, vision, optical-illusion
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# Question
Title: Is there any evidence for a bias towards perceiving darker surfaces as 'figure' rather than 'ground'?
Given that surfaces which capture attention are more likely to be perceived as figures (or figures attract attention more than ground does?), is there a bias associated with the luminance of a surface? For example, we often see dark figures (*e.g.*, text) on white paper.

Do you know of any literature to suggest a bias where darker surfaces are shown to attract attention more effectively than lighter surfaces (or *vice versa*)?

Or, alternatively, is there data available on a possible bias where figure-ground segmentation is more likely to occur for a dark figure on a white ground (or *vice versa*)?

# Answer
> 1 votes
**Short answer**
From my personal experience, I do not think darker surfaces are regarded preferably as the object, and light surfaces as the background.

**Background**
I have been pondering on this question for so long that I decided to post *an* answer. Perhaps it will draw attention from others who can give a more definitive answer.

This answer was inspired by this question on the **Rubin Vase Illusion**. It is an **ambiguous figure/ground illusion** which is thought to depend on the visual system analyzing scenes in terms of object (figure) and background (ground). You can see a vase when you regard the faces as background and *vice versa*. In the Fig. 1 below I have posted two versions of this illusion where the black and white portions are reversed. Personally, and hence anecdotally, I do not perceive a clear difference in the perception of the vase versus faces between both figures. Hence, based on this anecdotal evidence I tend to believe that the definition of figure and ground is independent on color (shades of gray in this case). I couldn't find references for the flip-flop rates or vase-versus-face perception time on the two stimuli, unfortunately. In all, what a great question!

Fig. 1. Contrast-inverted Rubin Illusions. sources: Winkler *et al*. (2006) (left panel) and Russel & Dowey (2014) (right panel)

**References**
**-** Russel & Dowey, *Psychology: An Introduction* (2014)
**-** Winkler *et al*. *Eur J Neurosci* (2006); **24**(2): 625–34

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Tags: cognitive-psychology, perception, vision
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title: Do cats exhibit the bouba/kiki effect?

text:
# Question
Title: Do cats exhibit the bouba/kiki effect?
I was fascinated when I first read Ramachandran's article about kiki bouba effect, and I was wondering if cats experience the same thing... As Ramachandran proved, our angular gyrus is responsible for this phenomenon, and I found a part of cat's brain, named FAES, which has neurons that spike for auditory and visual stimuli. Does anyone know if they experience it?

# Answer
> 7 votes
The bouba/kiki effect is the phenomenon that about 95% of subjects assign the name *bouba* to a blobby form, and the name *kiki* to a pointy shape (Fig. 1).

Fig. 1. Kiki and bouba, at least in 95% of the people. source: Synesthesia Test

It is thought that the reason behind the strong preference is that the sharp changes in visual direction of the lines in the left-hand panel in Fig. 1 mimics the sharp phonemic inflections of the sound *kiki*, as well as the sharp inflection of the tongue on the palate. Ramachandran poses that the bouba/kiki effect provides a clue for understanding the origins of proto-language, for it suggests that there sounds are mapped on to objects. Ramachandran poses that the representation of certain lip and tongue movements in motor brain areas are mapped in non-arbitrary ways onto certain sound inflections and phonemic representations in auditory regions and the latter in turn may have links to an external object’s visual appearance. These factors may have co-evolved, forming a possible origin of proto-language (Ramachandran & Hubbard, 2001).

To get to your question: cats can't talk. Their vocalizations are relatively restricted, adding up to 16 different sounds. They include the familiar meows, hissing when angry and purring when happy. The purring comes from deep within the body and isn't related to speech at all. The hissing sounds a bit like an /h/ and the meows include more varieties. However, the variability in 'meows' is largely due to **intonations** (source: The Independent), and not so much the phonemes. Phonemes are: '\[...\] sound\[s\], or set of similar speech sounds, which are perceived as a single distinctive sound by speakers of the language or dialect in question. For example, the "c/k" sounds in cat and kitten represent the English phoneme /k/.

Human speech is extremely diverse and is produced by the interplay of various organs, includes lip, tongue and glottal movements that change the way the vocal cords produce sounds. There are 36 phonemes (speech sounds) recognized in English.

The bouba/kiki effect hinges strongly on the phonemes /b/ and /k/ and, perhaps, /i/ and /ou/. Both in Ramachandran & Hubbard's experiment (bouba/kiki) (Ramachandran & Hubbard, 2001) and the original study by Kohler (baluba/takete) (reviewed shortly in *Ozturk et al*. (2013)).

Cats don't have that kind of repertoire of phonemes. So regardless the similarity in some brain areas, I dare to say a bouba/kiki or baluba/takete effect can never be found in cats. I realize this is a rather mechanistic approach to the question and I am indeed not saying that cats cannot experience **synesthesia**. But that's another question...

**References**
**-** Ozturk *et al*., *J Exp Child Psychol* (2013); **114**: 173–86
**-** Ramachandran & Hubbard, *J Consciousness Studies* (2001); **8**(12): 3–34

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Tags: neuroscience, perception, vision, cross-modal
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title: What exactly is Emotional Reasoning?

text:
# Question
Title: What exactly is Emotional Reasoning?
Emotional Reasoning, a cognitive distortion discovered by Aaron T. Beck, as stated on Wikipedia:

> Emotional reasoning is a cognitive process by which a person concludes that his/her emotional reaction proves something is true, regardless of the observed evidence. For example, even though a spouse has shown only devotion, a person using emotional reasoning might conclude, "I know my spouse is being unfaithful because I feel jealous."

If I go to an haunted place, and I become really anxious there, so my emotions are representing my thoughts about that place. So it's simple: you feel the way you think. How does Emotional Reasoning fit in this scene, or is it something else?

# Answer
The quote you gave was from the beginning of Wikipedia article on Emotional Reasoning and if you read further down in that article it tells you that

> Beck believed that emotional reasoning stemmed from negative thoughts that were uncontrollable and happened without effort.

Emotional Reasoning is a cognitive distortion which amplifies the effects of other cognitive distortions and it is a style of unhelpful thinking whereby you base your view of situations, yourself, or others, on the way you are thinking. What you are thinking and feeling **could** be rational but with this situation you are thinking irrationally as there is no hard factual evidence to support the thoughts.

You might think "I feel like an idiot, therefore I am an idiot"; "I feel guilty, therefore I must have done something bad"; "I feel inadequate, therefore I must be a worthless person"; "I'm furious with you, therefore you must have been acting badly and trying to take advantage of me"

Or just as in the question but phrased in this way, "I feel jealous, therefore it must be true that my spouse is being unfaithful".

With Emotional Reasoning you are reacting to what you alone are witnessing. The proposed situation regarding a haunted house making you feel anxious is not Emotional Reasoning. You are feeling anxious because you are apprehensive of what might happen if you encounter a ghost/spirit some other people have said they have witnessed.
> 3 votes

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Tags: cognitive-psychology, depression
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# Question
Title: Is satisficing conceptualised as being unconscious/automatic, or conscious/volitional?
I haven't found anything that speaks directly to this question, but here is the account Simon (1990) p9 provides of satisficing

> If the task domain has little structure or the structure is unknown to us, we apply so-called "weak methods," which experience has shown to be useful in many domains, but which may still require us to search a good deal. One weak method is satisficing--using experience to construct an expectation of how good a solution we might reasonably achieve, and halting search as soon as a solution is reached that meets the expectation.

Simon, H. A. (1990). Invariants of human behavior. Annual review of psychology, 41(1), 1-20.

# Answer
Satisficing is goal directed and satisficers intend to achieve satisfactory results. Therefore, satisficing seems to involve conscious choices being made.

However, in Unconscious Thought Theory (UTT), unconscious thought produces superior decisions compared to conscious thought when decision making is complex and there are paragraphs of Nelson and Winter (1982) that indicate that satisficing can be achieved from a sequence of mechanical, automatic steps of rule following.

Therefore looking at both H.A. Simon's conception and the findings from Nelson and Winter, satisficing can be either conscious or unconscious.
> 2 votes

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Tags: consciousness, bias
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# Question
Title: Method/Unit for measuring activity in specific frequency band for EEG
This may be more of a signal processing question but I'm looking to measure and compare activity in different frequency bands for each sensor. Unfortunately, all papers I've looked at simply refer to "alpha activity" without specifying how this was calculated.

Is there any standard method or "best practice" to measure the level of activity? Is it simply the average energy in the band (sum of the square of the absolute of the signal?)

Any help with this would be appreciated.

# Answer
How you analyse your data depends a bit on how you did your time-frequency decomposition.

If you're using a fast Fourier transform, you will likely cut out the temporal window of interest prior to analysis, and your power estimate will be a single value (per subject and/or condition) within this time window. For example, alpha wave desynchronisation is likely to kick in something like 100 ms after the onset of a tone, and you might be interested in its power between then and 300 ms. This is based on theory and literature, there is no single answer. But if you do cut out a time window in advance like this, make sure that the time window of interest is an exact multiple of the size of the cycle you are looking at! (e.g. a multiple of 1/10th of a second for 10 Hz.) Otherwise you might get some nasty artifacts.

What you will then end up with is one data point per subject and condition, per EEG sensor. Some people pre-select a group of sensors based on the literature, and look at average power across these sensors. In that case you can use any of the standard parametric statistics to test your hypotheses.

Alternatively, you might adopt a sliding time window or similar approach (see here), where you get an estimation of how power develops over time (per sensor and frequency band). In that case your data space is larger, and the usual way to constrain it is to use cluster-based permutation tests which are nonparametric. This will give you back clusters of significant differences across time and/or sensors (this means groups of successive time points or sensors near each other that show an experimental effect). Again, whether you want to average across sensors is a theoretical question. You can also decide to average across time using this approach, and to end up with a single data point per subject/condition as above. This approach is not particularly temporally precise - the data will be a bit smeared across time - but it gives you a better overview of what is going on in the brain and in which frequency bands the interesting effects might lie.

As for the unit, I prefer to convert raw power to decibel, because the scale is symmetric around zero and comparable across experiments. So, 10\*log10 of the power in your signal. If you're using a baseline, make it an absolute baseline (it's equivalent to a relative baseline for raw power, which is the standard).
> 2 votes

# Answer
To do this in EEGLAB, you are going to want to read this: sccn.ucsd.edu/wiki/Chapter\_11:\_Timefrequency\_decomposition. Your "level of activity" in a given frequency band is the magnitude of the frequency representation in that frequency band at a given point in time.

Really, though, EEGLAB is very heavily geared towards ICA analysis of whole brain activity, not of frequency analysis of single electrodes. If you want to do single electrode frequency analysis in Matlab, I would suggest using chronux (http://chronux.org): functions such as mtspectrumc will give you the frequency spectrum and then you can just take the magnitude of the spectrum in your preferred frequency band as your "level of activity" of that frequency band. See http://chronux.org/chronuxFiles/filesReleases/manual.pdf Section 2.2.1
> 0 votes

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Tags: eeg, signal-processing
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# Question
Title: What is the neurological basis of bipolar disorder?
Many sources claim that bipolar disorder is associated with problems in the homeostasis of excitatory neurotransmitters.

Is this true? What are the leading theories about neurological causes for bipolar disorder?

# Answer
> 4 votes
The exact cause of bipolar disorder is unknown (source: NHS). It is believed that there are a number of interacting physical, environmental and social factors that may cause bipolar disorder to develop.

* **Chemical imbalance in the brain**: Bipolar disorder is believed to be the result of chemical imbalances in the brain, and **noradrenaline** has been implicated (Young *et al*., 1994). Noradrenalin (norepinephrine) in the central nervous system regulates arousal and modulates reward circuitry and positive reinforcement. Many antidepressant drugs target noradrenergic projections to alleviate symptoms of depression (Trevino *et al*, 2012). There is evidence that episodes of **mania** may occur when levels of noradrenaline are too high, and episodes of **depression** may be the result of noradrenaline levels becoming too low (source: NHS). Reduced serotonin levels have been found too, which is a general hallmark of depression and not specifically related to bipolar disorder (Young *et al*., 1994).
* **Genetics**: bipolar disorder tends to run in families (Lichtenstein *et al*., 2009. The family members of a person with the condition have an increased risk of developing it themselves. However, no single gene is responsible for bipolar disorder. Instead, a number of genetic and environmental factors are thought to act as triggers (sources: NHS and Mayo Clinic).
* **Triggers**: A stressful circumstance or situation often triggers the symptoms of bipolar disorder, *e.g.*, physical, sexual or emotional abuse, or the death of a close family member. These life-altering events can cause episodes of depression at any time in a person's life. Bipolar disorder may also be triggered by physical illness, sleep disturbances, overwhelming problems in everyday life (sources: NHS and Mayo Clinic).

**References**
**-** Lichtenstein *et al*., *Lancet* (2009); **373**(9659): 234–9
**-** Trevino *et al*, *Encyclopedia of Human Behavior* (2012), 2nd ed.
**-** Young *et al*., *Biol Psychiatry* (1994); **35**(2): 121–7

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Tags: neuroscience, bipolar-disorder, etiology
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# Question
Title: Is intelligence (or mental ability) genetically transferred (inherited characteristic) from the parent to the offspring or is it an acquired trait?
The question is simple- whether our mental ability i.e. ability to acquire and store knowledge and comprehend and analyse the stored bits, an inherited trait (i.e. genetically transmitted from the parent to the offspring) or is it an acquired trait (depends on environmental, social factors)?

P.S. - Please attach the link of any reference/research (if any) with your answer.

# Answer
> 5 votes
You could start by reading "Intelligence: Knowns and Unknowns". This is a consensus article based on many of the world's leading researchers on intelligence.

Empirical research suggests that variations in intelligence is largely hereditary. Specifically estimates of heritability of intelligence at adulthood based on monozygotic twin samples who were reared appart suggests correlations of around .68 to .78 (see p.85 of the above article).

Of course, these estimates are typically based on samples growing up in the same country at a similar point in time. These estimates would be smaller if for example, monozygotic twins could be separated so that one twin grew up in a stone age society and another grew up in developed society with good education and health care.

Intelligence is something that develops over time. We can contrast acquired knowledge and skills (often called crystallised intelligence) with more abstract capacities (often called fluid intelligence). In particular, crystallised intelligence is predicted to improve more with schooling and general exposure to cultural learning experiences.

A lot more could be said about all this, but I recommend you just read the article, see below. It discusses these issue in accessible language and much greater depth:

https://www.mensa.ch/sites/default/files/Intelligence\_Neisser1996.pdf http://rcgd.isr.umich.edu/life/Readings2007/Nisbett%20reading.pdf

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Tags: genetics
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title: Is the Flynn effect autism?

text:
# Question
Title: Is the Flynn effect autism?
I've seen a lot of claims related to this:

1. Mild forms of autism increase IQ
2. IQ scores abruptly increased after 1979, when the MMR vaccine was introduced
3. The Flynn Effect was mainly on nonverbal IQ
4. Large IQ gains occurred in East Asia and Kenya along with introduction of vaccination
5. There may be a nonlinear effect, such that the increasing levels of vaccination in the 80s and 90s reduced IQ
6. The largest IQ gains occurred in racial groups with the lowest autism rates

Is there scientific proof for a relationship between IQ, autism and vaccines?

# Answer
The Flynn effect refers to the tendency over the last century or so for IQ scores to increase each generation by a few points.

There is no link between vaccination and autism. It is pseudo-scientific myth, which has dangerous consequences for public health. see discussion here.

I'm no expert in autism research, but in general, children with autism have lower IQ. I'm also not entirely clear how much the increasing rate of autism is a diagnostic change versus real change in prevalence (but I'll leave that to someone else). If there was a change, in real prevalence, then it would be an interesting question as to what might be causing it. One explanation that seems more plausible to me is that parental age is correlated with autism rates and that has certainly been increasing in the developed world. But this is not my area of expertise, so I'm not trying to present a definitive answer.

There are many plausible explanations for the Flynn effect related to societal level changes in nutrition, health, education, technology, parenting practices, educational strategies, screening of foetuses, and so forth. It's also interesting to ponder how much the change is related to the latent trait of intelligence, and how much is related to test taking skill. In some respects we are seeing similar societal level changes in height and life expectancy. Presumably, a whole range of societal changes could be culminating in what we see in terms of group-level IQ change.

Declines in the rate of intergenerational increases in IQ in particular subgroups may be related to some form asymptotic process. I.e., there is a point at which further IQ gains become more difficult to achieve for a society. In contrast, as social groups move from extreme disadvantage to less disadvantage, the gains may be quite noticeable. For example, I've read that the gap between black and white IQ scores in the United States has been reduced in recent years (based on greater inter-generational increases in IQ for blacks than for whites). And this in some sense speak to what the focus is on gain scores. Even if one social group has poorer environmental conditions (health, education, nutrition, etc.) than another, if the relative improvement in those conditions over a generation or two has been greater, we might still expect a greater gain.
> 8 votes

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Tags: abnormal-psychology, iq, autism
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# Question
Title: Does studying flashcards, both front to back and back to front, decrease retention opposed to only memorizing one way?
From this spaced repetition type flashcard user manual one can, "create cards that go in both directions (e.g., both “ookii”→“big” and “big”→“ookii”)."

In other words, would studying two flashcards (both with the same content but in reverse order, lessen the benefits of studying right at the periphery (i.e., spaced repetition)?

---

Here is a related question: Are spaced flashcards effective for learning?

Any comments with relevant studies is welcome--along with help. Feel free to edit or add to any idea to make the question less unclear.

# Answer
> 3 votes
No, it just makes the intervals suboptimal. Either **bury the card** if the opposite side came recently or change the card to the direction it will usually appear. (Sometimes it will be the description first.) The forgetting curve, memorizing right at the periphery, will still go back up:

There is also the study done by Glenberg Smith & Green about this...

Anki is programmed to deal with similar "sibling" cards The algorithm will **bury them**--except when learning...

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Tags: memory, long-term-memory, semantic-memory
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# Question
Title: How to recognize people with high need for cognition?
In my own little study I am trying to describe the personalities of different persons I know personally, by adding traits to them.

Among other traits, I am looking for those who have a high need for cognition (http://en.wikipedia.org/wiki/Need\_for\_cognition).

My challenge is: Those 3 people that I know have high NFC are all introverts, who don't tell others much of their thoughts. This means you need to know them very well or for a long time in order to recognize their NFC. This again implies that I don't really know for sure if anyone else I know have high NFC....

This makes me question 2 things:

1. Is there any correlation between NFC and extraversion?
2. Is there any way to recognize or measure people on NFC, without asking them questions? Maybe some kind of typical behavior or attitude for these people?

# Answer
> 5 votes
Assessing someone's personality without questionnaires can be done, an interesting "manual" is the book "Snoop" by Sam Gosling. Note, though, that Gosling limits himself to the Big 5, so he teaches how to recognize Openness to Experience (from someone's room: variety of topics in bookcase) but does not explicitly address Need for Cognition. But Gosling's book would be a decent place to start if you want to learn to assess personality factors without questionnaires.

Another book I'd recommend is Daniel Nettle's book "Personality", since terms like "introversion" mean different things to different people. For Nettle (and I guess mainstream psychology) introversion is relatively straightforward: it is basically (relatively) low sensitivity to positive emotions. However, 'laypeople' may consider a person an introvert if he or she is shy - but shyness is usually more related to neuroticism than to introversion. And an author like Susan Cain ("Quiet") seems to define introversion as what Nettle would call a combination of "true" introversion, neuroticism (shyness) and openness to experience/need for cognition. So if one would follow Cain's description, one would naturally link need for cognition to introversion, while 'scientific' psychology would not proclaim that.

That being said, personality factors tend to interact - extraverts may go to parties more often, so have less time to read books, and may therefore 'know less', causing others to underestimate their Need for Cognition.

Personally, if I would want to try to assess someone's need for cognition, I'd probably look at Openness, possibly substracting for supernatural beliefs like astrology or crop circles being caused by aliens, and for strict dogmatism/unquestioning deference to authority. If I can have a long debate with someone about a topic, without the other person saying things like 'because I say so' or 'that is obvious', or 'it is true since my intuition says so', or 'this (topic) is irrelevant', I'd guess the other would be relatively high on Need for Cognition. That being said, until the day that we can precisely define Need for Cognition as a sum of genes or the amplitude of a certain brainwave or the relative size of say the anterior cingulate cortex, there's always the risk that NfC itself is some kind of mixture of curiosity, enjoyment of thinking, culture of the parental home etcetera and assessment is skewed by for example the mood that the other person happens to be in.

So on your questions:

1. As far as I know, there is no relation between extraversion and Need for Cognition.
2. One may be able to guess a very approximate level of NfC if one has information about a person (level of education, political preference, interior of office, hobbies, the level of detail he/she discusses things in, width of interests) but if someone is a painfully shy and private person it may simply not be possible; I doubt you can read NfC from the shape of one's nose or such...

# Answer
> 4 votes
Like IQ, one's NFC is primarily judged by psychometric self-evaluation rather than behavior. The way in which we recognize NFC from a behavioral standpoint is to recognize the ways in which they seem to produce behaviors that a NFC psychometric test would evaluate.

In other words, if you want to recognize high NFC in others, you might want to familiarize yourself with the questions and traits that psychometric tests associate with high NFC. For example, this test asks questions that are representative of high NFC. So if you were to recognize someone who might answer 'yes' to "I usually end up deliberating about issues even when they do not affect me personally", or "I find satisfaction in deliberating hard and for long hours", then you could most likely recognize someone with high NFC.

Other behaviors may be less subtle. For example:

> \[Those with high need for cognition\] like to engage in complex, inquisitive, and analytical thoughts. They feel intrinsically motivated to devote effort to cognitive endeavors, striving to understand objects, events, and individuals. These individuals are less inclined to be biased by superficial factors, such as the appearance of speakers or social comparisons. In addition, they are more inclined to enjoy some experience if their expectations were low.
>
> Interestingly, both need for cognition, as well as need for affect--the motivation to experience strong emotions--increase the likelihood that people will become transported into these narratives (Thompson & Haddock, 2012). If need for cognition is elevated, people contemplate the tales more extensively, and appreciate the complexity of narratives, both of which facilitate transportation. If need for affect is elevated, people enjoy the emotions that transportation can evoke. The implication of this possibility is that need for cognition can, in some instances, increase the susceptibility of people to messages. For example, if an advertisement presents a narrative, need for cognition can facilitate transportation and thus diminish the likelihood of counterarguments. In contrast, if an advertisement presents a series of facts, instead of a narrative, transportation is precluded, and need for cognition could increase the likelihood of counterarguments.

Insofar as NFC and extraversion is concerned, there appears to be a positive correlation between need for cognition, openness, and conscientiousness. Thus, it is represented by openness to new and novel ideas and a willingness to engage in effortful thought (Verplanken, Hazenberg, & Palenewen, 1992). It does not appear to be linked to extroversion.

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Tags: cognitive-psychology, personality
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# Question
Title: Can I use data taken in a 5-point Likert Scale, and convert it as if it were taken as a 4-point Likert?
I made an error in my qualtrics survey, and used a 5-point Likert scale, when the measure was supposed to use a 4-point scale. I have collected a lot of my data for my dissertation, and am now very nervous. Do I have to go back and collect all of my data again?

# Answer
> 7 votes
In general, from my extensive experience, using a four or a five point response scale is not going to change much the psychometric properties of a typical psychological self-report scale (e.g., reliability and factor loadings). I also imagine that if you were to measure a multi-item scale with a four point version and a five point version that the correlation would be very close to the test-retest correlation you get with the five point scale.

More extreme changes (e.g., using a 2-point instead of a 5-point) or radically altering the response options would eventually start to create issues, but in the 4 to 7 point range, I think the effects would be subtle, especially if you are dealing with a multi-item scale.

The main issue you will have is that you wont be able to compare your descriptive statistics (e.g., means and standard deviations) with other authors who have used the standard 5-point scale. Whether this is an issue, depends on the aims of your analyses. If you are focused on relationships between variables (e.g., correlations, regressions, group differences, SEM, and so on), then whether you use a 4 or a 5-point scale is not going to make much difference. If you want to compare the means of your sample to the means of previous samples, or if there are particular scoring rules that involve the original metrics (e.g., some tests have cut-off scores used for classification), then you have more of a problem.

There are ways to approximate a rescaling. I.e., estimating what the means and SDs would have been had you used the 5-point instead of the 4-point scale.

```
rescaled_old_score =  (old_score - OLD_MIN) / (OLD_MAX - OLD_MIN)
new_score = rescaled_old_score * (NEW_MAX - NEW_MIN) + NEW_MIN

```

Here's what the function looks like in R:

```
rescale_item <- function(old_score, old_min = 1, old_max = 4, new_min = 1, new_max = 5) {
    rescaled_old_score <-  (old_score - old_min) / (old_max - old_min)
    rescaled_old_score * (new_max - new_min) + new_min
}

template <- data.frame(original = 1:4)
template$new <- round(rescale_item(template$original, 1, 4, 1, 5), 2)
template

```

which leads to the following rescaling:

```
  original  new
1        1 1.00
2        2 2.33
3        3 3.67
4        4 5.00

```

Of course, this is only an approximation. Better estimates of the mapping values could be obtained by administering the tests using both scales to the same sample.

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Tags: statistics, psychology
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# Question
Title: What does it mean when we say that "a neuron connects to a certain cortical layer"?
For example, if we say "a neuron connects to Layer V of the cortex", does it mean it synapses inside layer V, or does it imply that the soma of the neuron it synapses to is in Layer V (and it could synapse inside Layer II for example)?

# Answer
**Short answer**
In complicated matters like neural connections in a layered cortex, it is all about semantics. One should carefully place statements in their context and deduce their meaning.

**Background**
In Fig. 1 a schematic of the layering of the cortex is shown. The layers can be separated based on their histological and neurophysiological features:

* Layer I: the molecular layer, contains primarily axons running parallel (horizontal) to the cortical surface.
* Layer II, the external granular layer, is composed of a mixture of small granule cells and pyramidal cells. The apical dendrites of the pyramidal cells **extend into layer I** and their axons descend into and through the deeper cortical layers.
* Layer III, the external pyramidal layer, contains primarily pyramidal cells. Their **apical dendrites ascend into layer I** and their axons descend into and through the deeper layers.
* Layer IV, the internal granular layer, consists almost exclusively of stellate neurons. It can be divided into subdivisions in many neocortical areas. Layer IV is the primary target for ascending sensory information from the thalamus.
* Layer V, the internal pyramidal layer, consists predominantly of pyramidal cells. **Apical dendrites may extend upward one or two layers, and the larger pyramidal cells may have dendrites extending into layer I.**
* Layer VI, the multiform layer, contains an assortment of neuron types. The **dendrites of pyramidal cells may extend into layer I**. (source: Clinical Gate)

As the text in bold above shows, the apical dendrites of pyramidal cells can extend many layers. Hence, it is a matter of reading the text carefully to know what they are talking about.

In your example...

> \[A\] neuron connects to Layer V of the cortex...

...it would depend on the context, but in this isolated instance it simply reads that a neuron's axon terminates in layer V. Especially in histological texts a line like this would most likely have identified the axon and the axon terminal and have identified the layer where it terminates.

However, as said above, dendrites of pyramids *may* extend all the way up to layer I, so if a text would say...

> \[A\] neuron synapses onto a layer V neuron...

it is left undetermined exactly where that connection is made (can be layers I, II, III, IV, or V in the case of pyramidal cells).

What can be of help is the fact that when a text talks about...

> ...a layer V neuron

...you can safely assume that its cell body is located in layer V, as a cell's location is determined by its cell body. Its dendrites can be in any layer (especially of the larger pyramid cells) and its axon may traverse all layers.

Fig. 1. Layers in the cortex. source: Clinical Gate
> 5 votes

# Answer
Both are correct, technically, neurons a lined and positioned through synaptic connections and so logically each layer should comprise both the soma of neurons as well as the neurites for synaptic connections that can or may extend outside its layer and protrude its network outside. I highly recommend studying and understanding the processes and actions that are underscored in neural activity in the visual cortex.

http://www.ncbi.nlm.nih.gov/books/NBK10884/

PS. brain has 6 layers, try picturing fetal neurons climbing up radial glia stalks that transcend layers during fetal development!
> -2 votes

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Tags: theoretical-neuroscience, neural-network, neuroanatomy
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# Question
Title: How is an action potential conducted across axonal branches in a neuron?
As the action potential travels in the dendrite towards the cell body, it may encounter axonal branches. What happens at the branch? What makes it go to the cell body instead of other dendrite?

Also, as the action potential travel from the axon to its branches, does it go to only one or all terminals? If it goes to only one terminal, how is it decided which terminal it has to go?

# Answer
> 3 votes
Often action potentials arise not until the initial segment of the axon, sometimes referred to as the axon hillock. This has to do with a critical density of voltage-gated sodium channels needed for action potential generation (Kole *et al*., 2008). The way it is conducted though the dendrites is hence often by means of graded dendritic potentials.

Axon terminals are not "gated". The axon potential simply is conducted through all of them (see *e.g.*, Anesthesia Key), barred any refractory effects or inhibitory or excitatory inputs from axoaxonal connections.

<sub>**Reference**
**-** Kole *et al*., Nature Neurosci (2008); **11**: 178-86</sub>

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Tags: neuroscience, neurophysiology
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# Question
Title: Signal detection theory: How to calculate c' when d' is 0?
Reframed the original question to include more background information:

My experiment concerns the recall ability of individuals concerning information about animals. Within-subject design: Whether an animal is dangerous or safe (danger). Whether an animal lives in Africa or Australia (location). In the recall phase, participants had to identify the animals they saw as dangerous/safe, African/Australian. Responses were coded as Hit (stimuli danger, response danger), Miss (stimuli danger, response Safe), correct rejection (Stimuli safe, response safe) and finally false alarm (stimuli safe, response danger) We expected that sensitivity depends on the importance of the information to wellbeing (this has been found in other studies as well), but also that bias is affected by individual differences. D’ refers to sensitivity as it is the difference between the signal (danger) and noise distribution (safe). C refers to the bias (the criterion of the respondent, a tendency to say yes or no) and c’ is c relative to d’ . However, d’ in some cases is 0, when the proportion of hits (hits/(hits+misses) is equal to the proportion of false alarms (false alarms/(fa+correct rejections)) making it impossible to compute c’ (c/d'). As such, my question is whether there is a commonly used and supported correction? More information about signal detection theory and its use in cognitive sciences can be found here

Thank you for the comments so far, I hope the question is clearer now.

Original question: As described in Detection theory: A user's guide page 28, bias indicator c can be normalized into c' by dividing it by d'. In short, d' = z(H)-Z(FA); c = -0.5(z(H)+Z(FA)); c' = c/d'. However, in some of my cases d' is 0 (For instance, H=.72, FA =.72). Is there a standard correction that allows for the calculation of c'?

# Answer
> 1 votes
As you mention Macmillan and Creelman, they talk about 3 types of bias: c, c', and beta. As I said in this answer it normally does not matter which one you use since they are pretty easy to switch between. When d' is zero, then c' and beta are no longer as informative as c. I would suggest reporting c, possibly along with c', in this case. Alternatively, you could report hit and false alarm rates. If you only report c' and d', you will not be telling the whole story.

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Tags: signal-detection, psychophysics
---


# Question
Title: Who first proposed using ROC curves in a psychological context?
On Wikipedia it is written that

> In the 1950s, ROC curves were employed in psychophysics to assess human (and occasionally non-human animal) detection of weak signals.

Green and Swets (1966) is cited as attesting to that fact. I don't have any way of accessing that book, and nor would it necessarily constitute the first proposal of ROC curves for usage in psychology.

Green, D. M., & Swets, J. A. (1966). Signal detection theory and psychophysics. Society, 1, 521.

# Answer
> 4 votes
I worked out the answer to the question just as I was about to post it.

Swets (1973) writes of a 1954 conference that

> Peterson and Birdsall had presented it a year earlier in a technical report. So it is fair to say, from the vantage point of psychology, that Peterson and Birdsall showed us how to plot the data.

Unless Swets is mistaken, the answer is Peterson and Birdsall (1953).

Peterson, W. W., & Birdsall, T. G. The Theory of Signal Detectability (1953). Technical report No. 13, Electronic Defense Group, University of Michigan, Ann Arbor.

Swets, J. A. (1973). The relative operating characteristic in psychology. Science, 182(4116), 990-1000.

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Tags: terminology, signal-detection
---


# Question
Title: What is the difference between Machiavellianism and good negotiating/influence skills?
I have been addicted to 'Great courses' books for some time now and have read quite a few books on influence, social skills, conflict management, negotiating, etc.

Having basic knowledge in these areas I am now finding hard to see what is the difference between someone being Machiavellian and simply knowing how to negotiate, influence others.

One could argue that being moral is what separates the two however knowing about cultural differences across the world it would be quite hard to draw a line (we burned witches after having 'magna carta' and developed judiciary system for centuries) plus would inevitably have to delve in to moral philosophy... and eventually pretty much would end up having to make judgments subjectively.

**Is there an actual difference between Machiavellianism and good negotiating skills?**

# Answer
> 3 votes
The term "Machiavellianism" can be used to refer to adherence to a set of strategies and guidelines for manipulation (eg, "personally deliver good news but have bad news delivered by others"), a moral philosophy (eg, "the means justifies the ends"), or a personality trait (also called "Machiavellian intelligence"). Since you've posted this question on a cognitive science forum, I will focus on the latter definition.

Machiavellianism is measured (as any personality trait), using a self-report scale. This test, the Mach-IV, developed by Christie & Geis (1970), does not measure negotiation skills, but mostly focuses on social and moral attitudes and beliefs. As such, it would not normally be equated with any particular skills.

Fehr, Samson, & Paulhus (1992) review 17 years of research on Machiavellianism, including its association with persuasion:

> Several studies have found that high Machs are particularly adept at persuading others in bargaining situations.

The review also mentions some notable exceptions, including a study by Fry (1985), that showed that a simple visual barrier greatly reduces the influence of high Machs. A more recent review by Jones & Paulhus (2009) also agrees:

> ... high Mach IV scores do predict who will and who will not engage in interpersonal manipulation.

So although the term refers to a set of self-reported attitudes about social relationships, and not a measure of any particular skills, it would be reasonable to say that Machiavellianism ***correlates with*** negotiation skills.

For completeness, I should mention that the strong correlation is not an accident. In fact, as the review points out:

> ... the construct validity of Machiavellianism rests largely on the match between high Mach IV scores and actual pragmatic manipulation.

In other words, the test was written and adjusted to have this correlation, so it may be more accurate to say that Machiavellianism ***is validated by*** negotiation skills.

# Answer
> 0 votes
## Short answer

Negotiations can be subdivided into two categories: cooperative negotiations and competitive negotiations. Machiavellianism could be considered to be similar to competitive negotiations. It depends on the situation whether Machiavellianism can be considered as "good negotiation".

## Long answer

> Negotiation is a form of decision-making where two or more parties jointly search a space of possible solutions with the goal of reaching a consensus (p. 4, Gutmann & Maes, 1998).

The authors discuss two categories of negotiations that exist in a continuum: Competitive negotiations and cooperative negotiations. For competitive negotiations the goal is maximize your own reward. This often, if not always, comes at the cost of the reward of the other agent, i.e. the party you are negotiating with, because you have mutually exclusive goals. For example, if you must share 10 dollars, the goal of both agents would be to receive 10 dollars. With competitive negotiations, you try to come as close to that 10 dollar as possible.

During cooperative negotiations you try to find the best outcome for both parties. One reason to do so it that if you do not find the shared beneficial outcome, the reward could be even lower. For example, you again must share 10 dollars. However, if there is no consensus after some time, no money is given at all. Another example may be if there are repeated interactions (e.g. Bendor et al., 2001). If in the first negotiation you negotiate competitively, the other agent may be less inclined to accept sub-optimal outcomes in the second negotiation. Here is an old paper by Nash (1953) on cooperative negotiations (this is the same guy as from the Nash-equilibrium)

**Machiavellianism**
According to the Wikipedia page Machiavellianism is:

> the employment of cunning and duplicity in statecraft or in general conduct \[...\] characterized by a duplicitous interpersonal style, a cynical disregard for morality and a focus on self-interest and personal gain.

If I understand it correctly, Machiavellianism is thus clearly a competitive negotiation style in which the only goal is to maximize your own utility at the expense of the other agent.

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**Is there an actual difference between Machiavellianism and good negotiating skills?**

It depends from what you considered "good" negotiation. A competitive (Machiavellian) negotiation does not always result in an optimal outcome, nor does a cooperative one. Only in particular situations you could argue that Machiavellianism is the most effective strategy. However, given that Machiavellianism constitues **a cynical disregard for morality**, my guts tell me that is is not "good".

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Tags: social-psychology, abnormal-psychology
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# Question
Title: The relationship between creativity and focus
From what I have read here and there, I've managed to stitch together some superficial understanding of focus and creativity. My understanding is that focus and creativity seem like opposites.

I've seen references (which all seem to originate from a coursera course on learning) to two distinct "modes of thought". One called 'Focused' and one called 'Diffuse'. In focused mode, we focus on doing something we already know how to do. In Diffuse mode, we don't focus on a specific task we are instead searching for a way to do something, until we come up with an idea - it is at that point we focus on completing a task.

Whether this view of thought is scientifically grounded or not, there does seem to be some truth to it: the default mode network, whose activity is reduced during certain types of meditation (at least, according to wikipedia), from what i can understand is linked to creativity . The explanation of this default mode seems similar to the "diffuse" mode of thought.

It seems (at least, to me), that focus and creativity are opposites - which makes sense in some ways. But is it really so?

1. Are creativity and focus competitive as far as the brain structures that support these are concerned? That is, if I improve my ability to focus, will it interfere with my **ability** to be creative? This seems somewhat ridiculous to me, but I suspect it's only because I want to believe it isn't so. For the moment, my understanding is that creativity and focus are separate, and require "switching" between them, which leads to the next question:
2. Are creativity and focus competitive as far as brain activity goes? that is, if I try to focus on something right now, will it interfere with my ability to be creative? If I focus on solving a problem I know how to solve, I probably won't be looking for a creative solution (also, there is the Einstellung effect). But does the same mechanism responsible for maintaining or focus interfere with our ability to be creative at the moment?

# Answer
I can't really answer your questions as they relate to your ability to be creative. Also I'm unsure as to how 'focus' is defined, however, I know of research linking both attention and working memory to creativity which you may be able to draw conclusions from.

There is some mixed research to back the idea creativity and attention are linked; it has been hypothesised that individuals who suffer from ADHD (and thus a widened attentional focus) may have higher creative abilities than non ADHD individuals. One study on teens found that although those with ADHD out performed those without on tasks that involve overcoming the influence of examples, they showed a reduced capacity to generate a functional invention during an imagery task (Abraham et al 2006). White and Shah (2006) found similar results in adults and suggest than the disparity in creative ability may be linked to inhibition.

There has also been some research suggesting that creativity and capacity of working memory have opposing characteristics possibly in terms of diffuse attention. Working memory (WM) is an essential component for human higher order cognitive activities (large capacity for WM could come under 'focus'). Attention and WM share neural substrates and they are cognitively deeply associated (Awh and Jonides, 2001). Takeuchi et al used fMRI to investigate the link between WM and creativity and found that individual creativity, as measured by the divergent thinking test, is related to the inefficient reallocation of attention, congruent with the idea that diffuse attention is associated with individual creativity.

References:

Abraham, A., Windmann, S., Siefen, R., Daum, I., & Güntürkün, O. (2006). Creative thinking in adolescents with attention deficit hyperactivity disorder (ADHD). Child Neuropsychology, 12(2), 111-123.

White, H. A., & Shah, P. (2006). Uninhibited imaginations: creativity in adults with attention-deficit/hyperactivity disorder. Personality and Individual Differences, 40(6), 1121-1131.

Takeuchi, H., Taki, Y., Hashizume, H., Sassa, Y., Nagase, T., Nouchi, R., & Kawashima, R. (2011). Failing to deactivate: the association between brain activity during a working memory task and creativity. Neuroimage, 55(2), 681-687.

Awh, E., & Jonides, J. (2001). Overlapping mechanisms of attention and spatial working memory. Trends in cognitive sciences, 5(3), 119-126.
> 3 votes

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Tags: creativity, concentration
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# Question
Title: Where can I get data on lie detection and brain activity?
Are there databases or data sets that contain metrics about lie detection?

The data would include variables such as:

1. Did the subject lie? (0 or 1 variable)
2. Brain activity measures (fMRI, EEG) when subject was given question.

For example, was the hippocampus hyperactive when the subject was probed about a question? (Could be a discrete or continuous variable)

3. Metrics of the rest of the body

For example: Average heart rate, blood pressure level, level of various hormones, facial expressions, body posture, etc.

4. Any other metrics to describe people (remains to be seen if some of these variables would be useful): socio-economic status, age, race, gender, political affiliation, relgious affiliation, etc.

Does data involving, at least, points 1, 2, 3, exist? Point 4 would be a luxury, I suppose.

# Answer
> 4 votes
You might have trouble finding raw data but there have been plenty of studies looking at the neurological and physiological activity associated with deception, which may contain answers to your question:

A few examples: Ganis et al used fMRI and found that both types of lies (rehearsed & spontaneous) elicited more activation than telling the truth in anterior prefrontal cortices (bilaterally), the parahippocampal gyrus (bilaterally), the right precuneus, and the left cerebellum. At least in part, distinct neural networks support different types of deception.

Thackray & Orne published a pretty thorough comparison of lie detection methods.

Bradley & Janisse looked at threat and deception but discuss physiological response in depth.

Abe et al used PET scans to argue that we have distinct neural pathways for deception.

Additionally Sip et al discuss the efficacy of deception detection and studies summarising that

> The problems that bedevilled the old technology have not been eliminated by the new

References:

Ganis, G., Kosslyn, S. M., Stose, S., Thompson, W. L., & Yurgelun-Todd, D. A. (2003). Neural correlates of different types of deception: an fMRI investigation. Cerebral cortex, 13(8), 830-836.

Thackray, R. I., & Orne, M. T. (1968). A COMPARISON OF PHYSIOLOGICAL INDICES IN DETECTION OE DECEPTION. Psychophysiology, 4(3), 329-339.

Bradley, M. T., & Janisse, M. P. (1981). Accuracy demonstrations, threat, and the detection of deception: Cardiovascular, electrodermal, and pupillary measures. Psychophysiology, 18(3), 307-315.

Abe, N., Suzuki, M., Mori, E., Itoh, M., & Fujii, T. (2007). Deceiving others: distinct neural responses of the prefrontal cortex and amygdala in simple fabrication and deception with social interactions. Journal of Cognitive Neuroscience, 19(2), 287-295.

Sip, K. E., Roepstorff, A., McGregor, W., & Frith, C. D. (2008). Detecting deception: the scope and limits. Trends in cognitive sciences, 12(2), 48-53.

# Answer
> 3 votes
Simple answer. Yes, each researcher keeps data they use for research for at least 5 years, but their is no central database. You will need to request access to that data from the authors of any academic research on lie detection. If you read what I have written below then you can follow the links to the authors of the research and request their data. Although please be aware that they have may not wish to share their data.

The kinds of data you ask do exist but nobody takes all these measures in one experiment.

I feel inclined to provide a bit of background about lie detection research if you might indulge me.

Firstly, there is no such thing as a lie detector. The most sensitive equipment that could potentially be used to detect lies is electroencephalography (EEG), as it has high temporal resolution which would be necessary for lie detection. EEG equipment records electrical signals on the the scalp, which originate from the brain if you do it well, or from the surrounding muscles if you set the equipment up badly. Within the last 20 years research has tried and failed to accurately and constantly detect detection with both EEG and functional magnetic resonance imaging (fMRI). Hippocampal activity you will only really get with fMRI, although there are methods for EEG to get a weak signal. In general there are many problems using fMRI for lie detection, please see this link. Both methods are inconsistent at the detection of deception at the level of the individual, although some methods claim to have more success than others(please bare in mind this research was done in an Iranian university, meaning they are not known for their academic rigour at the time of writing). For instance this attached review reports that EEG analysis detection of 'deception' within p300 (this is a decision making signal that EEG detects) has been reported between 90 and 75% accurate in participant groups, looking at the data I would put it closer to 70%. This is not good enough for any uses by law enforcement.

With regards to questioning, law enforcement uses very specific techniques i.e. the cognitive interview so as not to negatively impact on recall. In addition these experiments are often done in the lab, where students are given a scenario and told to lie. This is very different from lying in the real world, for instance the signal of 'deception' in the p300 may get easily confused with normal decision making. Or the activity in certain neural areas may be normal functioning involved in recall rather than deception.

Without training lie detection is around 50%, in laboratory conditions. With regards to your other requests, galvanic skin response and heart rate changes have been used in the past with polygraphs. These are generally to reconsidered to be poor measures of lie detection as well.Another report here. Although some reports find remarkable findings, such as 80% lie detection, or if you are in china then they a reporting 95% lie detection. Although polygraph was debunked years ago to be at around 60%-65% accurate, see here for an excellent review. As the review points out false positives are a huge problem in polygraph techniques, as they are in other techniques too.

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Tags: cognitive-neuroscience, reference-request
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# Question
Title: What's the prevalence of interpersonal psychotherapy and cognitive behavior in the treatment of depression?
Is there any link, e-book, whitepaper that you can provide me to help me determine the prevalence of IPT and CBT amongst kids 7 - 12 years and adolescents 12 - 17 years who suffer from Major Depressive Disorder (MDD). This is for a clinical trial campaign we are doing due diligence for. I need to know if we can target enough number of participants to start a study.

# Answer
The mental health foundation (MHF) UK do some good work here, collecting data about prevalence of mental health problems and engagement with therapy. I have linked to a 2015 report which summarises a plethora of research on the depression, including MDD. You can follow the references to find information about the prevalence of MDD and engagement in therapy. For example, the paper references a 2006 meta-analysis of the prevalence of depression between 1965-1996 (USA statistics)..."overall prevalence estimates were: under 13, 2.8% (standard error (SE) .5%); 13–18 5.6% (SE .3%); 13–18 girls: 5.9% (SE .3%); 13–18 boys: 4.6% (SE .3%)" (Costello et al., 2006). A UK government report basically puts this prevalence at similar levels to the US. Going back to the USA, a 2014 report puts the incidence of depressive episode experiences at 11% of the US adolescent population. All I can say is that I'm glad I'm not a teenager anymore!

Therapy engagement and age is a bit more difficult to obtain, especially for interpersonal therapy in younger age groups. In the UK 38% of all therapy in primary healthcare (basically non-hospitalised patients) was CBT in 2013/14. In the annual NHS report for Improving Access to Psychological Therapies 2014/15(IAPT) puts this at 34% (1.2 million) by contrast interpersonal therapy was only around was just over 1% (40,000) of appointments. Under 18s age groups are not given, but it is reasonable to assume given the kind of therapy available for adults in the UK the rates would be similar for children, particularly because CBT training is more readily therapy. If your in the US it may be important to consider that therapy engagement maybe lower in younger age groups.

**TANGENT**
Worryingly and personally the most horrible statistic I have read all week is that depression in children is a risk factor to mortality comparable to smoking. However meta analysis have reported that CBT is 51-87% effective in treating depression. A Canadian report puts psychotherapy (CBT and IPT included) as .66 (cohen's D) more effective than no treatment at all in children with depression. The report does not compare success rates of either therapeutic technique. However a study has been planned to compare therapeutic treatments in children and adolescence, it has not been published yet. Rates of recovery in adults (which is often lower than children) may be an indicator, with IAPT reporting 58.4% recovery with CBT and 53.9% with IPT (remember the small sample size for IPT in IAPT). Within anxiety research cognitive therapy is found to be far more effective than IPT. One study appears to suggest that CBT is also more affective with depression than IPT, although a slightly older study found no significant difference, which looking at the IAPT data would seem to be more likely.

I hope that is helpful, I would also recommend looking at the USA based Nation Institute of Mental Health website, they have a lot of information and links to research.
> 1 votes

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Tags: depression
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# Question
Title: Is working memory equivalent to fluid intelligence?
Some report indicates that working memory capacity is equal to the g factor, so I'm wondering what is actual point of view on this among psychologists.

Colom, R., Abad, F. J., Rebollo, I., & Shih, P. C. (2005). Memory span and general intelligence: A latent variable approach. Intelligence, 33, 623–642.

# Answer
I would not go as far as saying that working memory (WM) is equal to g factor (gf). WM only accounts for 38% of variation in gf performance whether is no time pressure, this is not insignificant but it important to consider that holding information is important for any gf task. It has perviously been considered that the complexity of information required in different gf tasks would depend on WM capacity. For those that do not know: working memory (WM) is basically the capacity of information an individual can temporally hold at any one time. Anyhow the notion that complexity takes up more working memory and therefore is predictive of gf performance, in other words holding information in WM is thought to help us analyse and break it down to solve problems such as posed in gf tasks. This notion is does not appear to be supported, with research finding that the correlation between gf and WM being relatively consistent across task complexities.

So what is the function of this relationship? A 2011 fMRI study by Burgess et al strongly suggests that the relationship between WM and gf is to do with interference control, in their words..."Our findings suggest that the relationship between WM span and gF can be linked, at least in part, to a common dependence on mechanisms of interference control that reflect activation in a core set of brain regions centered on the lateral PFC and parietal cortex...these regions \[are\] fairly specific and selective in their predictive utility for explaining common variance in gF and WM span...We theorize that the exact brain regions and processes related to gF and WM span will likely depend upon the nature of processing required during the task, and the temporal dynamics of those task demands." Simply, the primary function of the relationship WM capacity and gf appears to be to focus on task. Interestingly from the area of hedonics we know that WM is predictive of how likely an individual is to respond their environment and motivational prompts such as food or alcohol. These motivational cues can be considered interference from long term goals such as avoiding eating or maintaining sobriety.
> 2 votes

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Tags: intelligence, working-memory
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title: Why do people tap their foot to music?

text:
# Question
Title: Why do people tap their foot to music?
When listening to music, I often see people tap their feet either to the main beat or the dominating rhythm of the music.

Why do people do this?

# Answer
> 7 votes
**Short Answer:**

People tap their feet due to increased activity in the cerebellum.

**Detailed Answer:**

There already is some evidence that music can release certain neurotransmitters, including dopamine. You can assume that people who tap their feet to the music, are in someway "pleased" by the music, meaning that their body goes into some sort of physiological joyride. Part of this joyride is an increased blood flow to the limbs, an increase in heart rate, dilated pupils, and most significantly a rise in activity of the cerebellum.

There is also the theory that music can have similar effects as drugs & addiction on the reward pathway of the brain. This pathway stimulates the flow of dopamine to the striatum, which is a part of the forebrain, activated by reward, motivation and addiction. In addition those dopamine levels can already peak milliseconds before something "special" in the song starts (e.g the bass drop, guitar solo, etc.), which strengthens the theory that our brain anticipates and predicts upcoming events (such as the memory prediction framework).

However, for example to songs the individual is completely unfamiliar with, the memory prediction framework may not be activated, therefore dopamine levels will not spike before the actual e.g. "drop", but after it happens, the striatum will be filled with dopamine. Furthermore, as mentioned in the beginning of the answer, the cerebellum gets more active as certain music is played, releasing neurotransmitters, and therefore the increased activity an individual is more likely to move their e.g. legs, because of a heightened motor-system.

**Sources:**

# Answer
> 4 votes
The short answer is that it is pleasurable.

Recent research from Witek et al (2014) sheds light on this. Their research on affective response and desire to move when listening to funk drum breaks showed that "syncopation seems to be an important structural factor in embodied and affective responses to groove". Here is their full PLOS article: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0094446)

This research rests on a longer history of research on the relationship to sound and motion. A nice framework that synthesizes this research was developed by Godøy et al. (2016) - http://www.tandfonline.com/doi/full/10.1080/09298215.2016.1184689

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Tags: cognitive-psychology, music, hearing
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# Question
Title: How does the intravenous administration of cholecystokinin provoke panic attacks?
**Background**

I recently read a paper (The James-Lange theory of emotions: a critical examination and an alternative theory), in which the James-Lange Theory was challenged by Walter Bradford Cannon.

Hence it was stated that:

> {Emotional responses can be distinguished by on the basis of autonomic activity., emotions were less intense when the brain was disconnected from the viscera} ... Some artificial manipulations of organ activity can induce emotions such as *intravenous administration of of cholecystokinin (a gastric peptide) which can provoke panic attacks*.

**Question**

What is the physiological process of intravenously inducing an emotion?

# Answer
Emotions are often linked to chemical activity in the brain. Neurotransmitters such as serotonin , dopamine, norepinephrine etc are linked to inducing emotional states, therefore if you can take a drug which will increase the amount of a transmitter then you will respond accordingly e.g. MDMA \> serotonin \> feeling of escstacy/happiness (Meyer & Quenzer, 2013).

In the case of Cholecystokinin (CCK), Singh et al found evidence suggesting that activation of the brain CCK-B receptor induces anxiety and that selective antagonists of this receptor represent a separate class of anxiolytic (relaxing) agents.

Simply:

* Inject drug
* drug reaches blood brain barrier
* drug crosses or is turned into drug that can cross (e.g. codiene \> morphine)
* drug turns into neurotransmitter/ or precursor to (e.g. 5HTP \> serotonin)
* binds to/ activates receptor this activation causes an emotional/physical response

This process varies depending on the drug but that is loosely it as I understand it. Much of this taken from the Meyers textbook, which I read a long time ago so feel free to correct me.

Singh, L., Lewis, A. S., Field, M. J., Hughes, J., & Woodruff, G. N. (1991). Evidence for an involvement of the brain cholecystokinin B receptor in anxiety. Proceedings of the National Academy of Sciences, 88(4), 1130-1133.

Meyer, J. S., & Quenzer, L. F. (2013). Psychopharmacology: Drugs, the brain, and behavior.
> 2 votes

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Tags: neuroscience, emotion, neuroanatomy
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# Question
Title: What effect can depression have on memory?
While a link has been shown that when a person is in a depressed episode there can be a negative effect on the individuals memory. (Hubbard et al, 2016). This shows that when a person is experiencing the symptoms of a depressive episode they can experience problems with memory and further impaired cognitive behavior(i.e slow to acknowledge new tasks, taking longer to comprehend sentences) Going beyond this point can depression have lasting memory effects after the symptoms have subdued and can memory be enhanced if someone is in a manic state?

Reference:

Hubbard, N. A., Hutchison, J. L., Turner, M., Montroy, J., Bowles, R. P., & Rypma, B. (2016). Depressive thoughts limit working memory capacity in dysphoria. Cognition and Emotion, 30(2), 193-209.

# Answer
My initial thought when reading this question is that it would an extremely difficult thing to pin down whether or not depression would affect memory in the long term this is due to a variety of confounding factors but the one that strikes me as most prominent is that major depression rarely goes untreated for a long period of time, in a population of people suffering with depression most are likely to have sought treatment as some point. Meaning that a study into the effects of depression in the long term would be very difficult to facilitate as it would be hard to infer whether the changes in memory function would be due to depression or the effects of treatment for depression such as SSRIs, MAOIs, electroconvulsive therapy, and others. Although, SSRIs have actually been found to improve memory (Harmer et al, 2002), and effects of ECT have been found to be temporary with people recovering by 6 months (Calev et al, 1991).

A link between depression and memory impairment is supported Burt, Zembar, & Niederehe conducted a meta analysis of 99 studies looking at depression and memory and found that:

> A significant, stable association between depression and memory impairment was revealed. Further analyses indicated, however, that it is likely that depression is linked to particular aspects of memory, the linkage is found in particular subsets of depressed individuals, and memory impairment is not unique to depression.

There is some evidence that people suffering from major depressive disorder have slightly different brain structure to neurotypical individuals. Brenner et al found that Patients with depression had a statistically significant 19% smaller left hippocampal volume than comparison subjects, without smaller volumes of comparison regions (amygdala, caudate, frontal lobe, and temporal lobe) or whole brain volume. It was not clear if this could change when the persons symptoms subdued, however to me it seemed like a permanent difference (obviously difficult to infer causality tho).

In terms of memory being enhanced in a manic state it appears that memory is much the same in a manic state as it is in a normal state (Glahn et al; Weingartner et al)

References

Bremner, J. D., Narayan, M., Anderson, E. R., Staib, L. H., Miller, H. L., & Charney, D. S. (2000). Hippocampal volume reduction in major depression. American Journal of Psychiatry, 157(1), 115-118.

Burt, D. B., Zembar, M. J., & Niederehe, G. (1995). Depression and memory impairment: a meta-analysis of the association, its pattern, and specificity. Psychological bulletin, 117(2), 285.

Calev, A., Nigal, D., Shapira, B., Tubi, N., Chazan, S., Ben-Yehuda, Y., ... & Lerer, B. (1991). Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions. The Journal of nervous and mental disease, 179(9), 526-533.

Glahn, D. C., Bearden, C. E., Cakir, S., Barrett, J. A., Najt, P., Serap Monkul, E., ... & Soares, J. C. (2006). Differential working memory impairment in bipolar disorder and schizophrenia: effects of lifetime history of psychosis. Bipolar disorders, 8(2), 117-123.

Harmer, C. J., Bhagwagar, Z., Cowen, P. J., & Goodwin, G. M. (2002). Acute administration of citalopram facilitates memory consolidation in healthy volunteers. Psychopharmacology, 163(1), 106-110.

Weingartner, H., Miller, H., & Murphy, D. L. (1977). Mood-state-dependent retrieval of verbal associations. Journal of Abnormal Psychology, 86(3), 276.
> 5 votes

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Tags: cognitive-psychology, psychiatry, depression, thought, bipolar-disorder
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