Instruct: Given a question, retrieve documents that answer the question.
Query: How much dopamine is in the human brain?
Dopaminergic neurons (dopamine-producing nerve cells) are comparatively few in number—a total of around 400,000 in the human brain—and their cell bodies are confined in groups to a few relatively small brain areas. However their axons project to many other brain areas, and they exert powerful effects on their targets. These dopaminergic cell groups were first mapped in 1964 by Annica Dahlström and Kjell Fuxe, who assigned them labels starting with the letter "A" (for "aminergic"). In their scheme, areas A1 through A7 contain the neurotransmitter norepinephrine, whereas A8 through A14 contain dopamine. The dopaminergic areas they identified are the substantia nigra (groups 8 and 9); the ventral tegmental area (group 10); the posterior hypothalamus (group 11); the arcuate nucleus (group 12); the zona incerta (group 13) and the periventricular nucleus (group 14).
In neuroscience, glutamate refers to the anion of glutamic acid in its role as a neurotransmitter: a chemical that nerve cells use to send signals to other cells. It is by a wide margin the most abundant excitatory neurotransmitter in the vertebrate nervous system. It is used by every major excitatory function in the vertebrate brain, accounting in total for well over 90% of the synaptic connections in the human brain. It also serves as the primary neurotransmitter for some localized brain regions, such as cerebellum granule cells.
Glutamate receptors are synaptic and non synaptic receptors located primarily on the membranes of neuronal and glial cells. Glutamate (the conjugate base of glutamic acid) is abundant in the human body, but particularly in the nervous system and especially prominent in the human brain where it is the body's most prominent neurotransmitter, the brain's main excitatory neurotransmitter, and also the precursor for GABA, the brain's main inhibitory neurotransmitter. Glutamate receptors are responsible for the glutamate-mediated postsynaptic excitation of neural cells, and are important for neural communication, memory formation, learning, and regulation.
Neuroscience has a unique perspective in that it can be applied in a broad range of disciplines, and thus the fields neuroscientists work in vary. Neuroscientists may study topics from the large hemispheres of the brain to neurotransmitters and synapses occurring in neurons at a micro-level. Some fields that combine psychology and neurobiology include cognitive neuroscience, and behavioural neuroscience. Cognitive neuroscientists study human consciousness, specifically the brain, and how it can be seen through a lens of biochemical and biophysical processes. Behaviorial neuroscience encompasses the whole nervous system, environment and the brain how these areas show us aspects of motivation, learning, and motor skills along with many others.
Alpha-synuclein is a protein that, in humans, is encoded by the "SNCA" gene. It is abundant in the brain while smaller amounts are found in the heart, muscles, and other tissues. In the brain, alpha-synuclein is found mainly at the tips of nerve cells (neurons) in specialized structures called presynaptic terminals. Within these structures, alpha-synuclein interacts with phospholipids and proteins. Presynaptic terminals release chemical messengers, called neurotransmitters, from compartments known as synaptic vesicles. The release of neurotransmitters relays signals between neurons and is critical for normal brain function.
The MAOIs work by inhibiting the monoamine oxidase enzymes that, as the name suggests, break down the monoamine neurotransmitters. This leads to increased concentrations of most of the monoamine neurotransmitters in the human brain, serotonin, norepinephrine, dopamine and melatonin. The fact that they are more efficacious than the newer generation antidepressants is what leads scientists to develop newer antidepressants that target a greater range of neurotransmitters. The problem with MAOIs is that they have many potentially dangerous side-effects such as hypotension, and there is a risk of food and drug interactions that can result in potentially fatal serotonin syndrome or a hypertensive crisis. Although selective MAOIs can reduce, if not eliminate these risks, their efficacy tends to be lower.
Glutamate is a major constituent of a wide variety of proteins; consequently it is one of the most abundant amino acids in the human body. Under ordinary conditions enough is obtained from the diet that there is no need for any to be synthesized. Nevertheless, glutamate is formally classified as a non-essential amino acid, because it can be synthesized from alpha-Ketoglutaric acid, which is produced as part of the citric acid cycle by a series of reactions whose starting point is citrate. Glutamate cannot cross the blood-brain barrier unassisted, but it is actively transported into the nervous system by a high affinity transport system, which maintains its concentration in brain fluids at a fairly constant level.
Axons transmit signals to other neurons by means of specialized junctions called synapses. A single axon may make as many as several thousand synaptic connections with other cells. When an action potential, traveling along an axon, arrives at a synapse, it causes a chemical called a neurotransmitter to be released. The neurotransmitter binds to receptor molecules in the membrane of the target cell.
Synapses are the key functional elements of the brain. The essential function of the brain is cell-to-cell communication, and synapses are the points at which communication occurs. The human brain has been estimated to contain approximately 100 trillion synapses; even the brain of a fruit fly contains several million. The functions of these synapses are very diverse: some are excitatory (exciting the target cell); others are inhibitory; others work by activating second messenger systems that change the internal chemistry of their target cells in complex ways. A large number of synapses are dynamically modifiable; that is, they are capable of changing strength in a way that is controlled by the patterns of signals that pass through them. It is widely believed that activity-dependent modification of synapses is the brain's primary mechanism for learning and memory.
Since glutamate is the most abundant and major excitatory neurotransmitter in the brain, pathophysiological changes in glutamatergic signaling are likely to affect neurobehavioral plasticity, information processing and large-scales changes in functional brain connectivity.Ketamine, a fast-acting general anesthetic derived from phencyclidine and use as a pediatric inductor, plays a non-well known role in the neural network dynamics at the healthy brain . The administration of ketamine in abnormal brain has the potential of reduce the increased function of the networks that are seen in depression. The therapeutic potential of ketamine may be explained by reversing disturbances in the glutamatergic system and restoring parts of a disrupted neurobehavioral homeostasis where several structural, metabolic, and functional abnormalities have taken place. Long term ketamine treatments lead to cognitive impairment including problems of short-term memory, visual and verbal memory. On the other hand, short term treatments are generally well tolerated and any damage may be reversible.
The brain of the domesticated cat is about long, and weighs . If a typical cat is taken to be long with a weight of , then the brain would be at 0.91% of its total body mass, compared to 2.33% of total body mass in the average human. Within the encephalization quotient proposed by Jerison in 1973, values above 1 are classified big brained, while values lower than 1 are small brained. The domestic cat is attributed a value of between 1–1.71 relative to human value that is 7.44–7.8. The largest brains in the Felidae family are those of the tigers in Java and Bali, of which the largest relative brain size within the "panthera" is the "tigris". It is debated whether there exists a causal relationship between brain size and intelligence in vertebrates. Correlations have been shown between these factors in a number of experiments. However, correlation does not imply causation. Most experiments involving the relevance of brain size to intelligence hinge on the assumption that complex behavior requires a complex (and therefore intelligent) brain; however, this connection has not been consistently demonstrated.
Glutamate is also a neurotransmitter (see below), which makes it one of the most abundant molecules in the brain. Malignant brain tumors known as glioma or glioblastoma exploit this phenomenon by using glutamate as an energy source, especially when these tumors become more dependent on glutamate due to mutations in the gene "IDH1".
Thewissen’s current work involves counting neurons in bowhead and beluga whale brain samples, to assess brain function, in Utqiagvik—formerly Barrow—Alaska. Though the size of the brains of sperm whales and killer whales are larger than those of any other organism, including humans, a better measure of brain function is to determine how many neurons there are in the brain. Suzana Herculano-Houzel has developed a method of counting of neurons of human and other animals' brains and the relation between the cerebral cortex area and thickness and number of cortical folds. Humans and other primates pack about twice the number of neurons in a cubed inch of brain as most other mammals.
The adrenal medulla () is part of the adrenal gland. It is located at the center of the gland, being surrounded by the adrenal cortex. It is the innermost part of the adrenal gland, consisting of cells that secrete epinephrine (adrenaline), norepinephrine (noradrenaline), and a small amount of dopamine in response to stimulation by sympathetic preganglionic neurons.
Abnormalities in the ascending and descending pathways involved in processing pain have been observed in fibromyalgia. 50% less stimulus is needed to evoke pain in those with fibromyalgia. A proposed mechanism for chronic pain is sensitization of secondary pain neurons mediated by increased release of proinflammatory cytokines and nitric oxide by glial cells. Inconsistent reports of decreased serum and CSF values of serotonin have been observed. There is also some data that suggests altered dopaminergic and noradrenergic signaling in fibromyalgia. Supporting the monoamine related theories is the efficacy of monoaminergic antidepressants in fibromyalgia.
The botulinum toxin can cause a severe flaccid paralytic disease in humans and other animals and is the most potent toxin known to mankind, natural or synthetic, with a lethal dose of 1.3–2.1 ng/kg in humans.
Findings reported in published studies of Tourette syndrome since 1999 have advanced TS science in the areas of genetics, neuroimaging, neurophysiology, and neuropathology. The TAA supports a clinical database that may help identify genes involved in Tourette syndrome, and the TSA International Genetic Consortium has collected a database on large extended families for future studies. Novel neuroimaging studies are being employed to study tic expression and functional or cognitive deficits in TS patients. Studies of Tourette's neurophysiology and neuropathology are attempting to link deficits in Tourette's to specific brain mechanisms, and have taken advantage of a brain bank sponsored by the TSA. Clinical trials have focused on understanding tic suppression, comorbid conditions, novel treatment approaches such as botulinum toxin, and targeted behavioral therapies. Controversy remains in the areas of deep brain stimulation and PANDAS.
The neuroscientist Donald Hebb (1904–1985) was the first to distinguish between short-term memory and long-term memory. According to current theories in neuroscience, things that we "notice" are stored in short-term memory for up to a few minutes; this memory depends on "reverberating" electrical activity in neuronal circuits, and is very easily destroyed by interruption or interference. Memories stored for longer than this are stored in "long-term memory". Whether information is stored in long-term memory depends on its "importance"; for any animal, memories of traumatic events are potentially important for the adaptive value that they have for future avoidance behavior, and hormones that are released during stress have a role in determining what memories are preserved. In humans, traumatic stress is associated with acute secretion of epinephrine and norepinephrine (adrenaline and noradrenaline) from the adrenal medulla and cortisol from the adrenal cortex. Increases in these facilitate memory, but chronic stress associated with prolonged hypersecretion of cortisol may have the opposite effect. The limbic system is involved in memory storage and retrieval as well as giving emotional significance to sensory inputs. Within the limbic system, the hippocampus is important for explicit memory, and for memory consolidation; it is also sensitive to stress hormones, and has a role in recording the emotions of a stressful event. The amygdala may be particularly important in assigning emotional values to sensory inputs.
The adrenal medulla is at the centre of each adrenal gland, and is surrounded by the adrenal cortex. The chromaffin cells of the medulla are the body's main source of the catecholamines adrenaline and noradrenaline, released by the medulla. Approximately 20% noradrenaline (norepinephrine) and 80% adrenaline (epinephrine) are secreted here.
Some 400 genes are shown to be brain-specific. In all neurons, ELAVL3 is expressed, and in pyramidal neurons, NRGN and REEP2 are also expressed. GAD1 – essential for the biosynthesis of the neurotransmitter GABA – is expressed in interneurons. Proteins expressed in glial cells are astrocyte markers GFAP, and S100B. Myelin basic protein, and the transcription factor, OLIG2 are expressed in oligodendrocytes.
This implied neuroplasticity during the critical period. However, Merzenich argued that neuroplasticity could occur beyond the critical period. His first encounter with adult plasticity came when he was engaged in a postdoctoral study with Clinton Woosley. The experiment was based on observation of what occurred in the brain when one peripheral nerve was cut and subsequently regenerated. The two scientists micromapped the hand maps of monkey brains before and after cutting a peripheral nerve and sewing the ends together. Afterwards, the hand map in the brain that they expected to be jumbled was nearly normal. This was a substantial breakthrough. Merzenich asserted that, "If the brain map could normalize its structure in response to abnormal input, the prevailing view that we are born with a hardwired system had to be wrong. The brain had to be plastic." Merzenich received the 2016 Kavli Prize in Neuroscience "for the discovery of mechanisms that allow experience and neural activity to remodel brain function."
She would like people to question research findings from neuroscientists in terms of effect size, she is critical of neuroscientists who describe "slight" statistical differences between the genders as "significant" differences in their findings. Rippon also says, if you are going to look at brain volume differences then you need to know how heavy and how tall those people are – a volume correction, otherwise the data is meaningless, and not all researchers, she says, do that. Another worry for Rippon is a publication bias, that publishers will only publish when a difference is found rather than publishing research proving there are no differences.
Dopamine (DA, a contraction of 3,4-dihydroxyphenethylamine) is an organic chemical of the catecholamine and phenethylamine families that plays several important roles in the brain and body. It is an amine synthesized by removing a carboxyl group from a molecule of its precursor chemical L-DOPA, which is synthesized in the brain and kidneys. Dopamine is also synthesized in plants and most animals. In the brain, dopamine functions as a neurotransmitter—a chemical released by neurons (nerve cells) to send signals to other nerve cells. The brain includes several distinct dopamine pathways, one of which plays a major role in the motivational component of reward-motivated behavior. The anticipation of most types of rewards increases the level of dopamine in the brain, and many addictive drugs increase dopamine release or block its reuptake into neurons following release. Other brain dopamine pathways are involved in motor control and in controlling the release of various hormones. These pathways and cell groups form a dopamine system which is neuromodulatory.
Coping with stress is a key aspect of rabbit behavior, and this can be traced to part of the brain known as ventral tegmental area (VTA). Dopaminergic neurons in this part of the brain release the hormone dopamine, generalized as a "feel-good" hormone. In humans, dopamine is released through a variety of acts, including sexual activity, substance abuse, and even eating chocolate. However, in rabbits, it is released as part of a coping mechanism while in a heightened state of fear or stress, and has a calming effect. Dopamine has also been found in the rabbit's medial prefrontal cortex, the nucleus accumbens, and the amygdala. Physiological and behavioral responses to human-induced tonic immobility (TI, sometimes termed "trancing" or "playing dead") have been found to be indicative of a fear-motivated stress state, confirming that the promotion of TI to try to increase a bond between rabbits and their owners—thinking the rabbits enjoy it—is misplaced. However, some researchers conclude that inducing TI in rabbits is appropriate for certain procedures, as it holds less risk than anesthesia.
Melanins are a family of dark-pigmented substances found in a wide range of organisms. Chemically they are closely related to dopamine, and there is a type of melanin, known as dopamine-melanin, that can be synthesized by oxidation of dopamine via the enzyme tyrosinase. The melanin that darkens human skin is not of this type: it is synthesized by a pathway that uses L-DOPA as a precursor but not dopamine. However, there is substantial evidence that the neuromelanin that gives a dark color to the brain's substantia nigra is at least in part dopamine-melanin.
In 1957 Kathleen Montagu demonstrated the presence of dopamine in the human brain; later that same year Carlsson also demonstrated that dopamine was a neurotransmitter in the brain and not just a precursor for norepinephrine. Carlsson went on to develop a method for measuring the amount of dopamine in brain tissues. He found that dopamine levels in the basal ganglia, a brain area important for movement, were particularly high. He then showed that giving animals the drug reserpine caused a decrease in dopamine levels and a loss of movement control. These effects were similar to the symptoms of Parkinson's disease. By administering to these animals L-Dopa, which is the precursor of dopamine, he could alleviate the symptoms. These findings led other doctors to try using L-Dopa in patients with Parkinson's disease, and it was found to alleviate some of the symptoms in the early stages of the disease. L-Dopa is still the basis for most commonly used means of treating Parkinson's disease.