Instruct: Given a question, retrieve documents that answer the question.
Query: How many neurotransmitters are there in the human brain?
There are dozens of other chemical neurotransmitters that are used in more limited areas of the brain, often areas dedicated to a particular function. Serotonin, for example—the primary target of antidepressant drugs and many dietary aids—comes exclusively from a small brainstem area called the raphe nuclei. Norepinephrine, which is involved in arousal, comes exclusively from a nearby small area called the locus coeruleus. Other neurotransmitters such as acetylcholine and dopamine have multiple sources in the brain, but are not as ubiquitously distributed as glutamate and GABA.
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".
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.
Dopamine is one of the chemicals that carries messages between brain cells. There is evidence that too much dopamine may be involved in the development of schizophrenia, but it’s still not clear how, or whether everyone diagnosed with schizophrenia has too much dopamine. Neuroleptic drugs (antipsychotics), which are sometimes used to treat schizophrenia, target the dopamine system.
As noradrenaline is an intermediate on the path to adrenaline, dopamine is on the path to noradrenaline (and hence adrenaline.) In 1957 dopamine was identified in the human brain by researcher Kathleen Montagu. In 1958/59 Arvid Carlsson and his group in the Pharmacology Department of the University of Lund, including the medical students Åke Bertler and Evald Rosengren, not only found dopamine in the brain, but also – like noradrenaline in Marthe Vogt's exemplary study – in uneven distribution, quite different from the distribution of noradrenaline. This argued for a function beyond an intermediate. The concentration was highest in the corpus striatum, which contained only traces of noradrenaline. Carlsson's group had previously found that reserpine, which was known to cause a Parkinsonism syndrome, depleted dopamine (as well as noradrenaline and serotonin) from the brain. They concluded that ″dopamine is concerned with the function of the corpus striatum and thus with the control of motor function″. Thus for the first time the reserpine-induced Parkinsonism in laboratory animals and, by implication, Parkinson's disease in humans was related to depletion of striatal dopamine. A year later Oleh Hornykiewicz, who had been introduced to dopamine by Blaschko and was carrying out a colour reaction on extracts of human corpus striatum in the Pharmacological Institute of the University of Vienna, saw the brain dopamine deficiency in Parkinson's disease ″with  own naked eye: Instead of the pink colour given by the comparatively high concentrations of dopamine in the control samples, the reaction vials containing the extracts of the Parkinson's disease striatum showed hardly a tinge of pink discoloration″.
Dopamine was first synthesized in 1910 by George Barger and James Ewens at Wellcome Laboratories in London, England and first identified in the human brain by Kathleen Montagu in 1957. It was named dopamine because it is a monoamine whose precursor in the Barger-Ewens synthesis is 3,4-dihydroxyphenylalanine (levodopa or L-DOPA). Dopamine's function as a neurotransmitter was first recognized in 1958 by Arvid Carlsson and Nils-Åke Hillarp at the Laboratory for Chemical Pharmacology of the National Heart Institute of Sweden. Carlsson was awarded the 2000 Nobel Prize in Physiology or Medicine for showing that dopamine is not only a precursor of norepinephrine (noradrenaline) and epinephrine (adrenaline), but is also itself a neurotransmitter.
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.
The scientific study of the nervous system increased significantly during the second half of the twentieth century, principally due to advances in molecular biology, electrophysiology, and computational neuroscience. This has allowed neuroscientists to study the nervous system in all its aspects: how it is structured, how it works, how it develops, how it malfunctions, and how it can be changed. For example, it has become possible to understand, in much detail, the complex processes occurring within a single neuron. Neurons are cells specialized for communication. They are able to communicate with neurons and other cell types through specialized junctions called synapses, at which electrical or electrochemical signals can be transmitted from one cell to another. Many neurons extrude a long thin filament of axoplasm called an axon, which may extend to distant parts of the body and are capable of rapidly carrying electrical signals, influencing the activity of other neurons, muscles, or glands at their termination points. A nervous system emerges from the assemblage of neurons that are connected to each other.
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.
All drugs and stimulants of the brain can affect how someone learns, consolidates, and retrieves certain memories. For example, cocaine blocks the reuptake of dopamine, a neurotransmitter in the brain, causing an increase of dopamine in the synaptic cleft. This will elicit a rewarding feeling of liberation and security that can become addictive to some people. Although, because of the increased dopamine levels in the brain, consolidation of memory can be affected which will then inhibit the chances of recovering that memory. Studies show that rats who were given cocaine were unable to perform motor tasks as successfully as the control group. Also, cannabis has also shown negative effects regarding the ability to spontaneously recover memories because the plasticity strength of the initial memories are so inhibited due to the reduced neurotransmitters in the synaptic cleft.
Amino acids are organic compounds containing amine (-NH) and carboxyl (-COOH) functional groups, along with a side chain (R group) specific to each amino acid. The key elements of an amino acid are carbon (C), hydrogen (H), oxygen (O), and nitrogen (N), although other elements are found in the side chains of certain amino acids. About 500 naturally occurring amino acids are known (though only 20 appear in the genetic code) and can be classified in many ways. They can be classified according to the core structural functional groups' locations as alpha- (α-), beta- (β-), gamma- (γ-) or delta- (δ-) amino acids; other categories relate to polarity, pH level, and side chain group type (aliphatic, acyclic, aromatic, containing hydroxyl or sulfur, etc.). In the form of proteins, amino acid residues form the second-largest component (water is the largest) of human muscles and other tissues. Beyond their role as residues in proteins, amino acids participate in a number of processes such as neurotransmitter transport and biosynthesis.
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.
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.
One is the neuroscientists' "objective" way. They dissect the brain with scalpel and microscope or look at it with brain scans and then trace neurochemical pathways. Neurology observes "mind" from outside, that is, by means of the neurological examination: questionnaires, the Boston Naming test or Wisconsin Sorting, bisecting lines, acting out how you use a screwdriver, and so on. Neurologists can compare the changes in psychological function that the neurological examination shows with the associated changes in the brain, either post mortem or by means of modern imaging technology.
Microglia are a collective type of neuroglia (glial cell) located throughout the brain and spinal cord., found to have 9 distinct subtypes with different functions, appearance, and presence. Microglia account for 10–15% of all cells found within the brain. As the resident macrophage cells, they act as the first and main form of active immune defense in the central nervous system (CNS). Microglia (and other neuroglia including astrocytes) are distributed in large non-overlapping regions throughout the CNS. Microglia are key cells in overall brain maintenance—they are constantly scavenging the CNS for plaques, damaged or unnecessary neurons and synapses, and infectious agents. Since these processes must be efficient to prevent potentially fatal damage, microglia are extremely sensitive to even small pathological changes in the CNS. This sensitivity is achieved in part by the presence of unique potassium channels that respond to even small changes in extracellular potassium.
Due to more recent Medical, Rehabilitation and ongoing results 'neuroplasticity' within the mechanics of our brains lead to re-arrangement of the brain's workings. These often result in the synapses arranging alternate routes, to achieve previous habits. Neuroplasticity is the brain's ability to reorganise itself by forming new neural connections throughout life. Neuroplasticity allows the neurons (nerve cells) in the brain to compensate for injury and disease and to adjust their activities in response to new situations or to changes in their environment.
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.
Kathleen Montagu (estimated birth between 1847 and 1907 – 28 March 1966) was the first researcher to identify dopamine in human brains. 
Working in Hans Weil-Malherbe’s laboratory at the Runwell Hospital outside London the presence of dopamine was identified by paper chromatography in the brain of several species, including a human brain. Her research was published in August 1957, followed and confirmed by Hans Weil-Malherbe in November 1957.
G protein-coupled receptors (GPCRs), also known as seven-transmembrane domain receptors, 7TM receptors, heptahelical receptors, serpentine receptor, and G protein-linked receptors (GPLR), comprise a large protein family of transmembrane receptors that sense molecules outside the cell and activate inside signal transduction pathways and, ultimately, cellular responses. G protein-coupled receptors are found only in eukaryotes, including yeast, choanoflagellates, and animals. The ligands that bind and activate these receptors include light-sensitive compounds, odors, pheromones, hormones, and neurotransmitters, and vary in size from small molecules to peptides to large proteins. G protein-coupled receptors are involved in many diseases, and are also the target of approximately 30% of all modern medicinal drugs.
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 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.
Three neurotransmitters that play important roles in adolescent brain development are glutamate, dopamine and serotonin. Glutamate is an excitatory neurotransmitter. During the synaptic pruning that occurs during adolescence, most of the neural connections that are pruned contain receptors for glutamate or other excitatory neurotransmitters. Because of this, by early adulthood the synaptic balance in the brain is more inhibitory than excitatory.
Neuropeptides modulate neuronal communication by acting on cell surface receptors. Many neuropeptides are co-released with other small-molecule neurotransmitters. The human genome contains about 90 genes that encode precursors of neuropeptides. At present about 100 different peptides are known to be released by different populations of neurons in the mammalian brain. Neurons use many different chemical signals to communicate information, including neurotransmitters, peptides, and gasotransmitters. Peptides are unique among these cell-cell signaling molecules in several respects. One major difference is that peptides are not recycled back into the cell once secreted, unlike many conventional neurotransmitters (glutamate, dopamine, serotonin). Another difference is that after secretion, peptides are modified by extracellular peptidases; in some cases, these extracellular cleavages inactivate the biological activity, but in other cases the extracellular cleavages increase the affinity of a peptide for a particular receptor while decreasing its affinity for another receptor. These extracellular processing events add to the complexity of neuropeptides as cell-cell signaling molecules.
The arcuate nucleus of the hypothalamus, a part of the brain, is the main regulatory organ for the human appetite. Many brain neurotransmitters affect appetite, especially dopamine and serotonin. Dopamine acts primarily through the reward centers of the brain, whereas serotonin primarily acts through effects on neuropeptide Y (NPY)/agouti-related peptide (AgRP) [stimulate appetite] and proopiomelanocortin (POMC) [induce satiety] neurons located in the arcuate nucleus. Similarly, the hormones leptin and insulin suppress appetite through effects on AgRP and POMC neurons.
Neurotransmitters are chemicals that are released at synapses when an action potential activates them—neurotransmitters attach themselves to receptor molecules on the membrane of the synapse's target cell, and thereby alter the electrical or chemical properties of the receptor molecules.
With few exceptions, each neuron in the brain releases the same chemical neurotransmitter, or combination of neurotransmitters, at all the synaptic connections it makes with other neurons; this rule is known as Dale's principle. Thus, a neuron can be characterized by the neurotransmitters that it releases. The great majority of psychoactive drugs exert their effects by altering specific neurotransmitter systems. This applies to drugs such as cannabinoids, nicotine, heroin, cocaine, alcohol, fluoxetine, chlorpromazine, and many others.