text:
Serotonin
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For other uses, see Serotonin (disambiguation).
Serotonin
Clinical data
Synonyms
5-HT, 5-Hydroxytryptamine, Enteramine, Thrombocytin, 3-(β-Aminoethyl)-5-hydroxyindole, Thrombotonin
Physiological data
Source tissues
raphe nuclei, enterochromaffin cells
Target tissues
system-wide
Receptors
5-HT1, 5-HT2, 5-HT3, 5-HT4, 5-HT5, 5-HT6, 5-HT7
Agonists
SSRIs, MAOIs (indirectly)
Precursor
5-HTP
Biosynthesis
Aromatic L-amino acid decarboxylase
Metabolism
MAO
Identifiers
IUPAC name[show]
3-(2-Aminoethyl)-1H-indol-5-ol
CAS Number
50-67-9
PubChem CID
5202
IUPHAR/BPS
5
ChemSpider
5013
KEGG
C00780
ECHA InfoCard
100.000.054
Serotonin
Names
IUPAC names
5-Hydroxytryptamine or
3-(2-Aminoethyl)indol-5-ol
Other names
5-Hydroxytryptamine, 5-HT, Enteramine; Thrombocytin, 3-(β-Aminoethyl)-5-hydroxyindole, Thrombotonin
Identifiers
CAS Number
50-67-9 Y
3D model (JSmol)
Interactive image
ChEBI
CHEBI:28790 Y
ChemSpider
5013 Y
ECHA InfoCard 100.000.054
IUPHAR/BPS
5
KEGG
C00780 Y
MeSH Serotonin
PubChem CID
5202
UNII
333DO1RDJY Y
InChI[show]
InChI=1S/C10H12N2O/c11-4-3-7-6-12-10-2-1-8(13)5-9(7)10/h1-2,5-6,12-13H,3-4,11H2 Y
Key: QZAYGJVTTNCVMB-UHFFFAOYSA-N Y
InChI=1/C10H12N2O/c11-4-3-7-6-12-10-2-1-8(13)5-9(7)10/h1-2,5-6,12-13H,3-4,11H2
Key: QZAYGJVTTNCVMB-UHFFFAOYAX
SMILES[show]
c1cc2c(cc1O)c(c[nH]2)CCN
Properties
Chemical formula
C10H12N2O
Molar mass 176.215 g/mol
Appearance White powder
Melting point 167.7 °C (333.9 °F; 440.8 K) 121–122 °C (ligroin)[3]
Boiling point 416 ± 30 °C (at 760 Torr)[1]
Solubility in water
slightly soluble
Acidity (pKa) 10.16 in water at 23.5 °C[2]
Dipole moment
2.98 D
Hazards
Safety data sheet External MSDS
Lethal dose or concentration (LD, LC):
LD50 (median dose)
750 mg/kg (subcutaneous, rat),[4] 4500 mg/kg (intraperitoneal, rat),[5] 60 mg/kg (oral, rat)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Y verify (what is Y N ?)
Infobox references
Serotonin (/ˌsɛrəˈtoʊnɪn, ˌsɪərə-/[6][7][8]) or 5-hydroxytryptamine (5-HT) is a monoamine neurotransmitter. Biochemically derived from tryptophan,[9] serotonin is primarily found in the gastrointestinal tract (GI tract), blood platelets, and the central nervous system (CNS) of animals, including humans. It is popularly thought to be a contributor to feelings of well-being and happiness.[10]
Approximately 90% of the human body's total serotonin is located in the enterochromaffin cells in the GI tract, where it is used to regulate intestinal movements.[11][12] The serotonin is secreted luminally and basolaterally which leads to increased serotonin uptake by circulating platelets and activation after stimulation, which gives increased stimulation of myenteric neurons and gastrointestinal motility.[13] The remainder is synthesized in serotonergic neurons of the CNS, where it has various functions. These include the regulation of mood, appetite, and sleep. Serotonin also has some cognitive functions, including memory and learning. Modulation of serotonin at synapses is thought to be a major action of several classes of pharmacological antidepressants.
Serotonin secreted from the enterochromaffin cells eventually finds its way out of tissues into the blood. There, it is actively taken up by blood platelets, which store it. When the platelets bind to a clot, they release serotonin, where it can serve as a vasoconstrictor and/or a vasodilator while regulating hemostasis and blood clotting. In high concentrations, serotonin acts as a vasoconstrictor by contracting endothelial smooth muscle directly or by potentiating the effects of other vasoconstrictors (e.g. angiotensin II, norepinephrine). The vasoconstrictive property is mostly seen in pathologic states affecting the endothelium such as atherosclerosis or chronic hypertension. In physiologic states, vasodilation occurs through the serotonin mediated release of nitric oxide from endothelial cells. Additionally, it inhibits the release of norepinephrine from adrenergic nerves.[14] Serotonin is also a growth factor for some types of cells, which may give it a role in wound healing. There are various serotonin receptors.
Serotonin is metabolized mainly to 5-HIAA, chiefly by the liver. Metabolism involves first oxidation by monoamine oxidase to the corresponding aldehyde. This is followed by oxidation by aldehyde dehydrogenase to 5-HIAA, the indole acetic acid derivative. The latter is then excreted by the kidneys.
Aside from mammals it is found in all bilateral animals including worms and insects, as well as in fungi and plants. Serotonin's presence in insect venoms and plant spines serves to cause pain, which is a side-effect of serotonin injection.[15] Serotonin is produced by pathogenic amoebae, and its effect in the human gut is diarrhea.[16] Its widespread presence in many seeds and fruits may serve to stimulate the digestive tract into expelling the seeds.[17]
Contents
[hide]
1 Functions
1.1 Perception of resource availability
1.2 Cellular effects
1.2.1 Receptors
1.2.2 Termination
1.2.3 Serotonylation
1.3 Nervous system
1.3.1 Ultrastructure and Function
1.3.2 Microanatomy
1.3.3 Psychological influences
1.4 Outside the nervous system
1.4.1 In the digestive tract (emetic)
1.4.2 Bone metabolism
1.4.3 Organ development
1.4.4 Cardiovascular growth factor
2 Pharmacology
2.1 Psychedelic drugs
2.2 Antidepressants
2.2.1 Serotonin syndrome
2.3 Antiemetics
2.4 Other
2.5 Methyl-tryptamines and hallucinogens
3 Comparative biology and evolution
3.1 Unicellular organisms
3.2 Plants
3.3 Invertebrates
3.4 Insects
3.5 Growth and reproduction
3.6 Aging and age-related phenotypes
4 Biochemical mechanisms
4.1 Biosynthesis
4.2 Effects of food content
5 History and etymology
6 See also
7 Notes
8 References
9 External links
Functions[edit]
Serotonin is a neurotransmitter and is found in all bilateral animals including insects.[18] Serotonin is also present in plants (phytoserotonin).[19]
Perception of resource availability[edit]
Serotonin mediates the animal's perceptions of resource; In less complex animals, such as some invertebrates, resources simply mean food availability.[20] In plants serotonin synthesis seems to be associated with stress signals.[19] In more complex animals, such as arthropods and vertebrates, resources also can mean social dominance.[21] In response to the perceived abundance or scarcity of resources, an animal's growth, reproduction or mood may be elevated or lowered. This may somewhat depend on how much serotonin the organism has at its disposal.[citation needed]
Cellular effects[edit]
Receptors[edit]
Main article: 5-HT receptor
The 5-HT receptors, the receptors for serotonin, are located on the cell membrane of nerve cells and other cell types in animals, and mediate the effects of serotonin as the endogenous ligand and of a broad range of pharmaceutical and hallucinogenic drugs. Except for the 5-HT3 receptor, a ligand-gated ion channel, all other 5-HT receptors are G-protein-coupled receptors (also called seven-transmembrane, or heptahelical receptors) that activate an intracellular second messenger cascade.[22]
Termination[edit]
Serotonergic action is terminated primarily via uptake of 5-HT from the synapse. This is accomplished through the specific monoamine transporter for 5-HT, SERT, on the presynaptic neuron. Various agents can inhibit 5-HT reuptake, including cocaine, dextromethorphan (an antitussive), tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs). A 2006 study conducted by the University of Washington suggested that a newly discovered monoamine transporter, known as PMAT, may account for "a significant percentage of 5-HT clearance".[23]
Contrasting with the high-affinity SERT, the PMAT has been identified as a low-affinity transporter, with an apparent Km of 114 micromoles/l for serotonin; approximately 230 times higher than that of SERT. However, the PMAT, despite its relatively low serotonergic affinity, has a considerably higher transport 'capacity' than SERT, "resulting in roughly comparable uptake efficiencies to SERT in heterologous expression systems."[this quote needs a citation] The study also suggests some SSRIs, such as fluoxetine and sertraline anti-depressants, inhibit PMAT but at IC50 values which surpass the therapeutic plasma concentrations by up to four orders of magnitude. Therefore, SSRI monotherapy is "ineffective" in PMAT inhibition. At present, no known pharmaceuticals are known to appreciably inhibit PMAT at normal therapeutic doses. The PMAT also suggestively transports dopamine and norepinephrine, albeit at Km values even higher than that of 5-HT (330–15,000 μmoles/L).[citation needed]
Serotonylation[edit]
Main article: Serotonylation
Serotonin can also signal through a nonreceptor mechanism called serotonylation, in which serotonin modifies proteins.[24] This process underlies serotonin's effects upon platelet-forming cells (thrombocytes) in which it links to the modification of signaling enzymes called GTPases that then trigger the release of vesicle contents by exocytosis.[25] A similar process underlies the pancreatic release of insulin.[24]
The effects of serotonin upon vascular smooth muscle tone (this is the biological function from which serotonin originally got its name) depend upon the serotonylation of proteins involved in the contractile apparatus of muscle cells.[26]
Binding profile of serotonin
Receptor
Ki (nM)[27]
Receptor function[Note 1]
5-HT1 receptor family signals via Gi/o inhibition of adenylyl cyclase.
5-HT1A 3.17 Memory[vague] (agonists ↓); learning[vague] (agonists ↓); anxiety (agonists ↓); depression (agonists ↓); positive, negative, and cognitive symptoms of schizophrenia (partial agonists ↓); analgesia (agonists ↑); aggression (agonists ↓); dopamine release in the prefrontal cortex (agonists ↑); serotonin release and synthesis (agonists ↓)
5-HT1B 4.32 Vasoconstriction (agonists ↑); aggression (agonists ↓); bone mass (↓). Serotonin autoreceptor.
5-HT1D 5.03 Vasoconstriction (agonists ↑)
5-HT1E 7.53
5-HT1F 10
5-HT2 receptor family signals via Gq activation of phospholipase C.
5-HT2A 11.55 Psychedelia (agonists ↑); depression (agonists & antagonists ↓); anxiety (antagonists ↓); positive and negative symptoms of schizophrenia (antagonists ↓); norepinephrine release from the locus coeruleus (antagonists ↑); glutamate release in the prefrontal cortex (agonists ↑); urinary bladder contractions (agonists ↑)[28]
5-HT2B 8.71 Cardiovascular functioning (agonists increase risk of pulmonary hypertension), empathy (via the spindle neurons or Von Economo neurons[29])
5-HT2C 5.02 Dopamine release into the mesocorticolimbic pathway (agonists ↓); acetylcholine release in the prefrontal cortex (agonists ↑); appetite (agonists ↓); antipsychotic effects (agonists ↑); antidepressant effects (agonists & antagonists ↑)
Other 5-HT receptors
5-HT3 593 Emesis (agonists ↑); anxiolysis (antagonists ↑).
5-HT4 125.89 Movement of food across the GI tract (agonists ↑); memory & learning (agonists ↑); antidepressant effects (agonists ↑). Signalling via Gαs activation of adenylyl cyclase.
5-HT5A 251.2 Memory consolidation.[30] Signals via Gi/o inhibition of adenylyl cyclase.
5-HT6 98.41 Cognition (antagonists ↑); antidepressant effects (agonists & antagonists ↑); anxiogenic effects (antagonists ↑[31]). Gs signalling via activating adenylyl cyclase.
5-HT7 8.11 Cognition (antagonists ↑); antidepressant effects (antagonists ↑). Acts by Gs signalling via activating adenylyl cyclase.
Nervous system[edit]
Serotonin system, contrasted with the dopamine system
The neurons of the raphe nuclei are the principal source of 5-HT release in the brain.[32] There are nine raphe nuclei, designated B1-B9, which contain the majority of serotonin-containing neurons (some scientists chose to group the nuclei raphes lineares into one nucleus), all of which are located along the midline of the brainstem, and centered on the reticular formation.[33][34] Axons from the neurons of the raphe nuclei form a neurotransmitter system reaching almost every part of the central nervous system. Axons of neurons in the lower raphe nuclei terminate in the cerebellum and spinal cord, while the axons of the higher nuclei spread out in the entire brain.
Ultrastructure and Function[edit]
The serotonin nuclei may also be divided into two main groups, the rostral and caudal containing three and four nuclei respectively. The rostral group consists of the caudal linear nuclei (B8), the dorsal raphe nuclei (B6 and B7) and the median raphe nuclei (B5, B8 and B9), that project into multiple cortical and subcortical structures. The caudal group consists of the nucleus raphe magnus (B3), raphe obscurus nucleus (B2), raphe pallidus nucleus (B1), and lateral medullary reticular formation, that project into the brainstem.[35]
Serotonergic pathway are involved in sensorimotor function, with pathways projecting both into cortical (Dorsal and Median Raphe Nuclei), subcortical, and spinal areas involved in motor activity. Pharmacological manipulation suggest that serotonergic activity increases with motor activity, while firing rates of serotonergic neurons increase with intense visual stimuli. The descending projections form a pathway that inhibits pain called the "descending inhibitory pathway" that may be relevant to disorder such as fibromyalgia, migraine and other pain disorders, and the efficacy of antidepressants in them.[36]
Serotonergic projections from the caudal nuclei are involved in regulating mood, emotion and hypo[37] or hyperserotonergic[38] states may be involved in depression and sickness behavior.
Microanatomy[edit]
Serotonin is released into the synapse, or space between neurons, and diffuses over a relatively wide gap (>20 µm) to activate 5-HT receptors located on the dendrites, cell bodies and presynaptic terminals of adjacent neurons.
When humans smell food, dopamine is released to increase the appetite. But, unlike in worms, serotonin does not increase anticipatory behaviour in humans; instead, the serotonin released while consuming activates 5-HT2C receptors on dopamine-producing cells. This halts their dopamine release, and thereby serotonin decreases appetite. Drugs that block 5-HT2C receptors make the body unable to recognize when it is no longer hungry or otherwise in need of nutrients, and are associated with weight gain,[39] especially in people with a low number of receptors.[40] The expression of 5-HT2C receptors in the hippocampus follows a diurnal rhythm,[41] just as the serotonin release in the ventromedial nucleus, which is characterised by a peak at morning when the motivation to eat is strongest.[42]
The amount of food that an animal acquires depends not only on food availability but also on the animal's ability to compete with others. This is especially true for social animals, where the stronger individuals might steal food from the weaker (this is not to say some non-social animals do not concern themselves with the needs of others or steal food from others[citation needed]). Thus, serotonin is involved not only in the perception of food availability but also in social rank.
In macaques, alpha males have twice the level of serotonin released in the brain than subordinate males and females (as measured by the levels of 5-Hydroxyindoleacetic acid (5-HIAA) in the cerebro-spinal fluid). Dominance status and cerebro-serotonin levels appear to be positively correlated. When dominant males were removed from such groups, subordinate males begin competing for dominance. Once new dominance hierarchies were established, serotonin levels of the new dominant individuals also increased to double those in subordinate males and females. The reason why serotonin levels are only high in dominant males but not dominant females has not yet been established.[43]
In humans, levels of 5-HT1A receptor activation in the brain show negative correlation with aggression,[44] and a mutation in the gene that codes for the 5-HT2A receptor may double the risk of suicide for those with that genotype.[45] Serotonin in the brain is not usually degraded after use, but is collected by serotonergic neurons by serotonin transporters on their cell surfaces. Studies have revealed nearly 10% of total variance in anxiety-related personality depends on variations in the description of where, when and how many serotonin transporters the neurons should deploy.[46]
Psychological influences[edit]
Serotonin has been implicated in cognition, mood, anxiety and psychosis, but strong clarity has not been achieved.[47][48]
Outside the nervous system[edit]
In the digestive tract (emetic)[edit]
The gut is surrounded by enterochromaffin cells, which release serotonin in response to food in the lumen. This makes the gut contract around the food. Platelets in the veins draining the gut collect excess serotonin.
If irritants are present in the food, the enterochromaffin cells release more serotonin to make the gut move faster, i.e., to cause diarrhea, so the gut is emptied of the noxious substance. If serotonin is released in the blood faster than the platelets can absorb it, the level of free serotonin in the blood is increased. This activates 5-HT3 receptors in the chemoreceptor trigger zone that stimulate vomiting.[49] The enterochromaffin cells not only react to bad food but are also very sensitive to irradiation and cancer chemotherapy. Drugs that block 5HT3 are very effective in controlling the nausea and vomiting produced by cancer treatment, and are considered the gold standard for this purpose.[50]
Bone metabolism[edit]
In mice and humans, alterations in serotonin levels and signalling have been shown to regulate bone mass.[51][52][53][54] Mice that lack brain serotonin have osteopenia, while mice that lack gut serotonin have high bone density. In humans, increased blood serotonin levels have been shown to be significant negative predictor of low bone density. Serotonin can also be synthesized, albeit at very low levels, in the bone cells. It mediates its actions on bone cells using three different receptors. Through 5-HT1B receptors, it negatively regulates bone mass, while it does so positively through 5-HT2B receptors and 5-HT2C receptors. There is very delicate balance between physiological role of gut serotonin and its pathology. Increase in the extracellular content of serotonin results in a complex relay of signals in the osteoblasts culminating in FoxO1/ Creb and ATF4 dependent transcriptional events.[55] These studies have opened a new area of research in bone metabolism that can be potentially harnessed to treat bone mass disorders.[56]
Organ development[edit]
Since serotonin signals resource availability it is not surprising that it affects organ development. Many human and animal studies have shown that nutrition in early life can influence, in adulthood, such things as body fatness, blood lipids, blood pressure, atherosclerosis, behavior, learning and longevity.[57][58][59] Rodent experiment shows that neonatal exposure to SSRI's makes persistent changes in the serotonergic transmission of the brain resulting in behavioral changes,[60][61] which are reversed by treatment with antidepressants.[62] By treating normal and knockout mice lacking the serotonin transporter with fluoxetine scientists showed that normal emotional reactions in adulthood, like a short latency to escape foot shocks and inclination to explore new environments were dependent on active serotonin transporters during the neonatal period.[63][64]
Human serotonin can also act as a growth factor directly. Liver damage increases cellular expression of 5-HT2A and 5-HT2B receptors, mediating liver compensatory regrowth (see Liver § Regeneration and transplantation)[65] Serotonin present in the blood then stimulates cellular growth to repair liver damage.[66] 5HT2B receptors also activate osteocytes, which build up bone[67] However, serotonin also inhibits osteoblasts, through 5-HT1B receptors.[68]
Cardiovascular growth factor[edit]
Main article: Cardiac fibrosis
Serotonin, in addition, evokes endothelial nitric oxide synthase activation and stimulates, through a 5-HT1B receptor-mediated mechanism, the phosphorylation of p44/p42 mitogen-activated protein kinase activation in bovine aortic endothelial cell cultures.[69] In blood, serotonin is collected from plasma by platelets, which store it. It is thus active wherever platelets bind in damaged tissue, as a vasoconstrictor to stop bleeding, and also as a fibrocyte mitotic (growth factor), to aid healing.[70]
Pharmacology[edit]
Several classes of drugs target the 5-HT system, including some antidepressants, antipsychotics, anxiolytics, antiemetics, and antimigraine drugs, as well as the psychedelic drugs and empathogens.
Psychedelic drugs[edit]
The psychedelic drugs psilocin/psilocybin, DMT, mescaline, psychedelic mushroom and LSD are agonists, primarily at 5HT2A/2C receptors.[71][72][73] The empathogen-entactogen MDMA releases serotonin from synaptic vesicles of neurons.[74]
Antidepressants[edit]
Main articles: SSRI and MAOI
Drugs that alter serotonin levels are used in treating depression, generalized anxiety disorder and social phobia. Monoamine oxidase inhibitors (MAOIs) prevent the breakdown of monoamine neurotransmitters (including serotonin), and therefore increase concentrations of the neurotransmitter in the brain. MAOI therapy is associated with many adverse drug reactions, and patients are at risk of hypertensive emergency triggered by foods with high tyramine content, and certain drugs. Some drugs inhibit the re-uptake of serotonin, making it stay in the synaptic cleft longer. The tricyclic antidepressants (TCAs) inhibit the reuptake of both serotonin and norepinephrine. The newer selective serotonin reuptake inhibitors (SSRIs) have fewer side-effects and fewer interactions with other drugs.[75]
Certain SSRI medications have been shown to lower serotonin levels below the baseline after chronic use, despite initial increases.[76] The 5-HTTLPR gene codes for the number of serotonin transporters in the brain, with more serotonin transporters causing decreased duration and magnitude of serotonergic signaling.[77] The 5-HTTLPR polymorphism (l/l) causing more serotonin transporters to be formed is also found to be more resilient against depression and anxiety.[78][79]
Serotonin syndrome[edit]
Main article: Serotonin syndrome
Extremely high levels of serotonin can cause a condition known as serotonin syndrome, with toxic and potentially fatal effects. In practice, such toxic levels are essentially impossible to reach through an overdose of a single antidepressant drug, but require a combination of serotonergic agents, such as an SSRI with an MAOI.[80] The intensity of the symptoms of serotonin syndrome vary over a wide spectrum, and the milder forms are seen even at nontoxic levels.[81]
Antiemetics[edit]
Some 5-HT3 antagonists, such as ondansetron, granisetron, and tropisetron, are important antiemetic agents. They are particularly important in treating the nausea and vomiting that occur during anticancer chemotherapy using cytotoxic drugs. Another application is in the treatment of postoperative nausea and vomiting.
Other[edit]
Some serotonergic agonist drugs cause fibrosis anywhere in the body, particularly the syndrome of retroperitoneal fibrosis, as well as cardiac valve fibrosis.[82] In the past, three groups of serotonergic drugs have been epidemiologically linked with these syndromes. These are the serotonergic vasoconstrictive antimigraine drugs (ergotamine and methysergide),[82] the serotonergic appetite suppressant drugs (fenfluramine, chlorphentermine, and aminorex), and certain anti-Parkinsonian dopaminergic agonists, which also stimulate serotonergic 5-HT2B receptors. These include pergolide and cabergoline, but not the more dopamine-specific lisuride.[83]
As with fenfluramine, some of these drugs have been withdrawn from the market after groups taking them showed a statistical increase of one or more of the side effects described. An example is pergolide. The drug was declining in use since it was reported in 2003 to be associated with cardiac fibrosis.[84]
Two independent studies published in the New England Journal of Medicine in January 2007, implicated pergolide, along with cabergoline, in causing valvular heart disease.[85][86] As a result of this, the FDA removed pergolide from the United States market in March 2007.[87] (Since cabergoline is not approved in the United States for Parkinson's Disease, but for hyperprolactinemia, the drug remains on the market. Treatment for hyperprolactinemia requires lower doses than that for Parkinson's Disease, diminishing the risk of valvular heart disease).[88]
Methyl-tryptamines and hallucinogens[edit]
For details on tryptamine neurotransmitters in humans, see Trace amine.
Several plants contain serotonin together with a family of related tryptamines that are methylated at the amino (NH2) and (OH) groups, are N-oxides, or miss the OH group. These compounds do reach the brain, although some portion of them are metabolized by monoamine oxidase enzymes (mainly MAO-A) in the liver. Examples are plants from the Anadenanthera genus that are used in the hallucinogenic yopo snuff. These compounds are widely present in the leaves of many plants, and may serve as deterrents for animal ingestion. Serotonin occurs in several mushrooms of the genus Panaeolus.[89]
Comparative biology and evolution[edit]
Unicellular organisms[edit]
Serotonin is used by a variety of single-cell organisms for various purposes. SSRIs have been found to be toxic to algae.[90] The gastrointestinal parasite Entamoeba histolytica secretes serotonin, causing a sustained secretory diarrhea in some people.[16][91] Patients infected with E. histolytica have been found to have highly elevated serum serotonin levels, which returned to normal following resolution of the infection.[92] E. histolytica also responds to the presence of serotonin by becoming more virulent.[93] This means serotonin secretion not only serves to increase the spread of enteamoebas by giving the host diarrhea but also serves to coordinate their behaviour according to their population density, a phenomenon known as quorum sensing. Outside the gut of a host, there is nothing that the entoamoebas provoke to release serotonin, hence the serotonin concentration is very low. Low serotonin signals to the entoamoebas they are outside a host and they become less virulent to conserve energy. When they enter a new host, they multiply in the gut, and become more virulent as the enterochromaffine cells get provoked by them and the serotonin concentration increases.
Plants[edit]
In drying seeds, serotonin production is a way to get rid of the buildup of poisonous ammonia. The ammonia is collected and placed in the indole part of L-tryptophan, which is then decarboxylated by tryptophan decarboxylase to give tryptamine, which is then hydroxylated by a cytochrome P450 monooxygenase, yielding serotonin.[94]
However, since serotonin is a major gastrointestinal tract modulator, it may be produced by plants in fruits as a way of speeding the passage of seeds through the digestive tract, in the same way as many well-known seed and fruit associated laxatives. Serotonin is found in mushrooms, fruits and vegetables. The highest values of 25–400 mg/kg have been found in nuts of the walnut (Juglans) and hickory (Carya) genera. Serotonin concentrations of 3–30 mg/kg have been found in plantains, pineapples, banana, kiwifruit, plums, and tomatoes. Moderate levels from 0.1–3 mg/kg have been found in a wide range of tested vegetables.[17]
Serotonin is one compound of the poison contained in stinging nettles (Urtica dioica), where it causes pain on injection in the same manner as its presence in insect venoms (see below). It is also naturally found in Paramuricea clavata, or the Red Sea Fan.[95]
Serotonin and tryptophan have been found in chocolate with varying cocoa contents. The highest serotonin content (2.93 µg/g) was found in chocolate with 85% cocoa, and the highest tryptophan content (13.27–13.34 µg/g) was found in 70–85% cocoa. The intermediate in the synthesis from tryptophan to serotonin, 5-hydroxytryptophan, was not found.[96]
Invertebrates[edit]
Serotonin functions as a neurotransmitter in the nervous systems of most animals. For example, in the roundworm Caenorhabditis elegans, which feeds on bacteria, serotonin is released as a signal in response to positive events, such as finding a new source of food or in male animals finding a female with which to mate.[97] When a well-fed worm feels bacteria on its cuticle, dopamine is released, which slows it down; if it is starved, serotonin also is released, which slows the animal down further. This mechanism increases the amount of time animals spend in the presence of food.[98] The released serotonin activates the muscles used for feeding, while octopamine suppresses them.[99] Serotonin diffuses to serotonin-sensitive neurons, which control the animal's perception of nutrient availability.
If lobsters are injected with serotonin, they behave like dominant individuals whereas octopamine causes subordinate behavior.[21] A crayfish that is frightened may flip its tail to flee, and the effect of serotonin on this behavior depends largely on the animal's social status. Serotonin inhibits the fleeing reaction in subordinates, but enhances it in socially dominant or isolated individuals. The reason for this is social experience alters the proportion between serotonin receptors (5-HT receptors) that have opposing effects on the fight-or-flight response.[clarification needed] The effect of 5-HT1 receptors predominates in subordinate animals, while 5-HT2 receptors predominates in dominants.[100]
Insects[edit]
Serotonin is evolutionary conserved and appears across the animal kingdom. It is seen in insect processes in roles similar to in the human central nervous system, such as memory, appetite, sleep, and behavior.[101][18] Locust swarming is mediated by serotonin, by transforming social preference from aversion to a gregarious state that enables coherent groups.[102] Learning in flies and honeybees is affected by the presence of serotonin.[103][104] Insect 5-HT receptors have similar sequences to the vertebrate versions, but pharmacological differences have been seen. Invertebrate drug response has been far less characterized than mammalian pharmacology and the potential for species selective insecticides has been discussed.[105]
Wasps and hornets have serotonin in their venom,[106] which causes pain and inflammation.[15] as do scorpions.[107]
If flies are fed serotonin, they are more aggressive; flies depleted of serotonin still exhibit aggression, but they do so much less frequently.[108]
Growth and reproduction[edit]
In the nematode C. elegans, artificial depletion of serotonin or the increase of octopamine cues behavior typical of a low-food environment: C. elegans becomes more active, and mating and egg-laying are suppressed, while the opposite occurs if serotonin is increased or octopamine is decreased in this animal.[20] Serotonin is necessary for normal nematode male mating behavior,[109] and the inclination to leave food to search for a mate.[110] The serotonergic signaling used to adapt the worm's behaviour to fast changes in the environment affects insulin-like signaling and the TGF beta signaling pathway,[111] which control long-term adaption.
In the fruit fly insulin both regulates blood sugar as well as acting as a growth factor. Thus, in the fruit fly, serotonergic neurons regulate the adult body size by affecting insulin secretion.[112][113] Serotonin has also been identified as the trigger for swarm behavior in locusts.[114] In humans, though insulin regulates blood sugar and IGF regulates growth, serotonin controls the release of both hormones, modulating insulin release from the beta cells in the pancreas through serotonylation of GTPase signaling proteins.[24] Exposure to SSRIs during Pregnancy reduces fetal growth.[115]
Genetically altered C. elegans worms that lack serotonin have an increased reproductive lifespan, may become obese, and sometimes present with arrested development at a dormant larval state.[116][117]
Aging and age-related phenotypes[edit]
Serotonin is known to regulate aging, learning and memory. The first evidence comes from the study of longevity in C. elegans.[118] During early phase of aging[vague], the level of serotonin increases, which alters locomotory behaviors and associative memory.[119] The effect is restored by mutations and drugs (including mianserin and methiothepin) that inhibit serotonin receptors. The observation does not contradict with the notion that the serotonin level goes down in mammals and humans, which is typically seen in late but not early[vague] phase of aging.
Biochemical mechanisms[edit]
Biosynthesis[edit]
The pathway for the synthesis of serotonin from tryptophan.
In animals including humans, serotonin is synthesized from the amino acid L-tryptophan by a short metabolic pathway consisting of three enzymes: tryptophan hydroxylase (TPH), aromatic amino acid decarboxylase (DDC) and pyridoxal phosphate. The TPH-mediated reaction is the rate-limiting step in the pathway. TPH has been shown to exist in two forms: TPH1, found in several tissues, and TPH2, which is a neuron-specific isoform.[120]
Serotonin can be synthesized from tryptophan in the lab using Aspergillus niger and Psilocybe coprophila as catalysts. The first phase to 5-hydroxytryptophan would require letting tryptophan sit in ethanol and water for 7 days, then mixing in enough HCl (or other acid) to bring the pH to 3, and then adding NaOH to make a pH of 13 for 1 hour. Asperigillus niger would be the catalyst for this first phase. The second phase to synthesizing tryptophan itself from the 5-hydroxytryptophan intermediate would require adding ethanol and water, and letting sit for 30 days this time. The next two steps would be the same as the first phase: adding HCl to make the pH = 3, and then adding NaOH to make the pH very basic at 13 for 1 hour. This phase uses the Psilocybe coprophila as the catalyst for the reaction.[121]
Serotonin taken orally does not pass into the serotonergic pathways of the central nervous system, because it does not cross the blood–brain barrier.[122] However, tryptophan and its metabolite 5-hydroxytryptophan (5-HTP), from which serotonin is synthesized, does cross the blood–brain barrier. These agents are available as dietary supplements, and may be effective serotonergic agents. One product of serotonin breakdown is 5-hydroxyindoleacetic acid (5-HIAA), which is excreted in the urine. Serotonin and 5-HIAA are sometimes produced in excess amounts by certain tumors or cancers, and levels of these substances may be measured in the urine to test for these tumors.
Effects of food content[edit]
See also: Tryptophan
Consuming purified tryptophan increases brain serotonin whereas eating foods containing tryptophan does not.[123] This is because the transport system which brings tryptophan across the blood-brain barrier is also selective for the other amino acids contained in protein sources.[122] High plasma levels of other large neutral amino acids compete for transport and prevent the elevated plasma tryptophan from increasing serotonin synthesis.
History and etymology[edit]
In 1935, Italian Vittorio Erspamer showed an extract from enterochromaffin cells made intestines contract. Some believed it contained adrenaline, but two years later, Erspamer was able to show it was a previously unknown amine, which he named "enteramine".[124] In 1948, Maurice M. Rapport, Arda Green, and Irvine Page of the Cleveland Clinic discovered a vasoconstrictor substance in blood serum, and since it was a serum agent affecting vascular tone, they named it serotonin.[125]
In 1952, enteramine was shown to be the same substance as serotonin, and as the broad range of physiological roles was elucidated, the abbreviation 5-HT of the proper chemical name 5-hydroxytryptamine became the preferred name in the pharmacological field.[126] Synonyms of serotonin include: 5-hydroxytriptamine, thrombotin, enteramin, substance DS, and 3-(β-Aminoethyl)-5-hydroxyindole.[127] In 1953, Betty Twarog and Page discovered serotonin in the central nervous system.[128]
See also[edit]
5-HT2c receptor agonist
Notes[edit]
Jump up ^ References are ignored for the functions of these receptors due to the fact they appear on the wikipedia pages for the specific receptor in question
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Jump up ^ Kaplan DD, Zimmermann G, Suyama K, Meyer T, Scott MP; Zimmermann; Suyama; Meyer; Scott (2008). "A nucleostemin family GTPase, NS3, acts in serotonergic neurons to regulate insulin signaling and control body size". Genes Dev. 22 (14): 1877–93. PMC 2492735  . PMID 18628395. doi:10.1101/gad.1670508. CS1 maint: Multiple names: authors list (link)
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Jump up ^ Anstey ML, Rogers SM, Ott SR, Burrows M, Simpson SJ; Rogers; Ott; Burrows; Simpson (2009). "Serotonin mediates behavioral gregarization underlying swarm formation in desert locusts". Science. 323 (5914): 627–30. Bibcode:2009Sci...323..627A. PMID 19179529. doi:10.1126/science.1165939. Lay summary – BBC News. CS1 maint: Multiple names: authors list (link)
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Jump up ^ SciFinder – Serotonin Substance Detail. Accessed (4 November 2012).[full citation needed]
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External links[edit]
Wikimedia Commons has media related to Serotonin.
5-Hydroxytryptamine MS Spectrum
Serotonin bound to proteins in the PDB
PsychoTropicalResearch Extensive reviews on serotonergic drugs and Serotonin Syndrome.
Molecule of the Month: Serotonin at University of Bristol
60-Second Psych: No Fair! My Serotonin Level Is Low, Scientific American
Serotonin Test Interpretation on ClinLab Navigator.
Gutknecht L; Jacob C; Strobel A; et al. (June 2007). "Tryptophan hydroxylase-2 gene variation influences personality traits and disorders related to emotional dysregulation". The International Journal of Neuropsychopharmacology. 10 (3): 309–20. PMID 17176492. doi:10.1017/S1461145706007437.
The Psychobiology of Serotonin Deficiency Syndrome
[show]
v
t
e
Neurotransmitters
Amino acid-derived
Major excitatory/inhibitory systems: Glutamate system: Agmatine
Aspartic acid (aspartate)
Cycloserine
Glutamic acid (glutamate)
Glutathione
Glycine
GSNO
GSSG
Kynurenic acid
NAA
NAAG
Proline
Serine; GABA system: GABA
GABOB
GHB; Glycine system: α-Alanine
β-Alanine
Glycine
Hypotaurine
Proline
Sarcosine
Serine
Taurine; GHB system: GHB
T-HCA (GHC)
Biogenic amines: Monoamines: 6-OHM
Dopamine
Epinephrine (adrenaline)
NAS (normelatonin)
Norepinephrine (noradrenaline)
Serotonin (5-HT); Trace amines:
3-Iodothyronamine
N-Methylphenethylamine
N-Methyltryptamine
m-Octopamine
p-Octopamine
Phenylethanolamine
Phenethylamine
Synephrine
Tryptamine
m-Tyramine
p-Tyramine; Others: Histamine
Neuropeptides: See here instead.
Lipid-derived
Endocannabinoids: 2-AG
2-AGE (noladin ether)
2-ALPI
2-OG
AA-5-HT
Anandamide (AEA)
DEA
LPI
NADA
NAGly
OEA
Oleamide
PEA
RVD-Hpα
SEA
Virodhamine (O-AEA)
Neurosteroids: See here instead.
Nucleobase-derived
Nucleosides: Adenosine system: Adenosine
ADP
AMP
ATP
Vitamin-derived
Cholinergic system: Acetylcholine
Miscellaneous
Gasotransmitters: Carbon monoxide (CO)
Hydrogen sulfide (H2S)
Nitric oxide (NO); Candidates: Acetaldehyde
Ammonia (NH3)
Carbonyl sulfide (COS)
Nitrous oxide (N2O)
Sulfur dioxide (SO2)
[show]
v
t
e
Serotonin receptor modulators
5-HT1
5-HT1A
Agonists: 8-OH-DPAT
Adatanserin
Amphetamine
Antidepressants (e.g., etoperidone, hydroxynefazodone, nefazodone, trazodone, triazoledione, vilazodone, vortioxetine)
Atypical antipsychotics (e.g., aripiprazole, asenapine, brexpiprazole, cariprazine, clozapine, lurasidone, quetiapine, ziprasidone)
Azapirones (e.g., buspirone, eptapirone, gepirone, perospirone, tandospirone)
Bay R 1531
Befiradol
BMY-14802
Cannabidiol
Dimemebfe
Dopamine
Ebalzotan
Eltoprazine
Enciprazine
Ergolines (e.g., bromocriptine, cabergoline, dihydroergotamine, ergotamine, lisuride, LSD, methylergometrine (methylergonovine), methysergide, pergolide)
F-11461
F-12826
F-13714
F-14679
F-15063
F-15599
Flesinoxan
Flibanserin
Flumexadol
Lesopitron
LY-293284
LY-301317
mCPP
MKC-242
Naluzotan
NBUMP
Osemozotan
Oxaflozane
Pardoprunox
Piclozotan
Rauwolscine
Repinotan
Roxindole
RU-24969
S-14506
S-14671
S-15535
Sarizotan
Serotonin (5-HT)
SSR-181507
Sunepitron
Tryptamines (e.g., 5-CT, 5-MeO-DMT, 5-MT, bufotenin, DMT, indorenate, N-Me-5-HT, psilocin, psilocybin)
TGBA01AD
U-92016A
Urapidil
Vilazodone
Xaliproden
Yohimbine
Antagonists: Atypical antipsychotics (e.g., iloperidone, risperidone, sertindole)
AV965
Beta blockers (e.g., alprenolol, carteolol, cyanopindolol, iodocyanopindolol, isamoltane, oxprenolol, penbutolol, pindobind, pindolol, propranolol, tertatolol)
BMY-7378
CSP-2503
Dotarizine
Ergolines (e.g., metergoline)
Flopropione
GR-46611
Isamoltane
Lecozotan
Mefway
Metitepine (methiothepin)
MIN-117 (WF-516)
MPPF
NAN-190
Robalzotan
S-15535
SB-649915
SDZ 216-525
Spiperone
Spiramide
Spiroxatrine
UH-301
WAY-100135
WAY-100635
Xylamidine
Unknown/unsorted: Acetryptine
Ergolines (e.g., ergometrine (ergonovine))
5-HT1B
Agonists: CGS-12066A
CP-93129
CP-94253
CP-122,288
CP-135807
Eltoprazine
Ergolines (e.g., bromocriptine, dihydroergotamine, ergotamine, methylergometrine (methylergonovine), methysergide, pergolide)
mCPP
RU-24969
Serotonin (5-HT)
Triptans (e.g., avitriptan, donitriptan, eletriptan, sumatriptan, zolmitriptan)
TFMPP
Tryptamines (e.g., 5-BT, 5-CT, 5-MT, DMT)
Vortioxetine
Antagonists: AR-A000002
Beta blockers (e.g., alprenolol, carteolol, isamoltane, oxprenolol, penbutolol, propranolol, tertatolol)
Elzasonan
Ergolines (e.g., metergoline)
GR-127935
Isamoltane
LY-393558
Metitepine (methiothepin)
SB-216641
SB-224289
SB-236057
Yohimbine
Unknown/unsorted: Ergolines (e.g., cabergoline, ergometrine (ergonovine), lisuride)
5-HT1D
Agonists: CP-122,288
CP-135807
CP-286601
Ergolines (e.g., bromocriptine, cabergoline, dihydroergotamine, ergotamine, LSD, methysergide)
GR-46611
L-694247
L-772405
mCPP
PNU-109291
PNU-142633
Serotonin (5-HT)
TGBA01AD
Triptans (e.g., almotriptan, avitriptan, donitriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan, zolmitriptan)
Tryptamines (e.g., 5-BT, 5-CT, 5-Et-DMT, 5-MT, 5-(nonyloxy)tryptamine, DMT)
Antagonists: Alniditan
BRL-15572
Elzasonan
Ergolines (e.g., metergoline)
GR-127935
Ketanserin
LY-310762
LY-367642
LY-393558
LY-456219
LY-456220
Metitepine (methiothepin)
Mianserin
Ritanserin
Yohimbine
Ziprasidone
Unknown/unsorted: Acetryptine
Ergolines (e.g., lisuride, lysergol, pergolide)
5-HT1E
Agonists: BRL-54443
Ergolines (e.g., methysergide)
Serotonin (5-HT)
Triptans (e.g., eletriptan)
Tryptamines (e.g., tryptamine)
Antagonists: Metitepine (methiothepin)
Unknown/unsorted: Ergolines (e.g., ergometrine (ergonovine), lysergol, methylergometrine (methylergonovine)
5-HT1F
Agonists: BRL-54443
CP-122,288
Ergolines (e.g., bromocriptine, lysergol, methylergometrine (methylergonovine) methysergide)
Lasmiditan
LY-334370
Serotonin (5-HT)
Triptans (e.g., eletriptan, naratriptan, sumatriptan)
Tryptamines (e.g., 5-MT)
Antagonists: Mianserin
Metitepine (methiothepin)
5-HT2
5-HT2A
Agonists: 25H/NB series (e.g., 25I-NBF, 25I-NBMD, 25I-NBOH, 25I-NBOMe, 25B-NBOMe, 25C-NBOMe, 25TFM-NBOMe, 2CBCB-NBOMe, 25CN-NBOH, 2CBFly-NBOMe)
2Cs (e.g., 2C-B, 2C-E, 2C-I, 2C-T-2, 2C-T-7, 2C-T-21)
2C-B-FLY
2CB-Ind
5-Methoxytryptamines (5-MeO-DET, 5-MeO-DiPT, 5-MeO-DMT, 5-MeO-DPT, 5-MT)
α-Alkyltryptamines (e.g., 5-Cl-αMT, 5-Fl-αMT, 5-MeO-αET, 5-MeO-αMT, α-Me-5-HT, αET, αMT)
AL-34662
AL-37350A
Bromo-DragonFLY
Dimemebfe
DMBMPP
DOx (e.g., DOB, DOC, DOI, DOM)
Efavirenz
Ergolines (e.g., 1P-LSD, ALD-52, bromocriptine, cabergoline, ergine (LSA), ergometrine (ergonovine), ergotamine, lisuride, LA-SS-Az, LSB, LSD, LSD-Pip, LSH, LSP, methylergometrine (methylergonovine), pergolide)
Flumexadol
Jimscaline
Lorcaserin
MDxx (e.g., MDA (tenamfetamine), MDMA (midomafetamine), MDOH, MMDA)
O-4310
Oxaflozane
PHA-57378
PNU-22394
PNU-181731
RH-34
Phenethylamines (e.g., lophophine, mescaline)
Piperazines (e.g., BZP, quipazine, TFMPP)
Serotonin (5-HT)
TCB-2
TFMFly
Tryptamines (e.g., 5-BT, 5-CT, bufotenin, DET, DiPT, DMT, DPT, psilocin, psilocybin, tryptamine)
Antagonists: 5-I-R91150
5-MeO-NBpBrT
AC-90179
Adatanserin
Altanserin
Antihistamines (e.g., cyproheptadine, hydroxyzine, ketotifen, perlapine)
AMDA
Atypical antipsychotics (e.g., amperozide, aripiprazole, asenapine, blonanserin, brexpiprazole, carpipramine, clocapramine, clorotepine, clozapine, fluperlapine, gevotroline, iloperidone, lurasidone, melperone, mosapramine, ocaperidone, olanzapine, paliperidone, quetiapine, risperidone, sertindole, zicronapine, ziprasidone, zotepine)
Cinanserin
CSP-2503
Deramciclane
Dotarizine
Eplivanserin
Ergolines (e.g., amesergide, LY-53857, LY-215840, mesulergine, metergoline, methysergide, sergolexole)
Fananserin
Flibanserin
Glemanserin
Irindalone
Ketanserin
KML-010
Landipirdine
LY-393558
mCPP
Medifoxamine
Metitepine (methiothepin)
MIN-101
MIN-117 (WF-516)
Naftidrofuryl
Nantenine
Nelotanserin
Opiranserin (VVZ-149)
Pelanserin
Phenoxybenzamine
Pimavanserin
Pirenperone
Pizotifen
Pruvanserin
Rauwolscine
Ritanserin
S-14671
Sarpogrelate
Serotonin antagonists and reuptake inhibitors (e.g., etoperidone, hydroxynefazodone, lubazodone, mepiprazole, nefazodone, triazoledione, trazodone)
SR-46349B
TGBA01AD
Teniloxazine
Temanogrel
Tetracyclic antidepressants (e.g., amoxapine, aptazapine, esmirtazapine, maprotiline, mianserin, mirtazapine)
Tricyclic antidepressants (e.g., amitriptyline)
Typical antipsychotics (e.g., chlorpromazine, fluphenazine, haloperidol, loxapine, perphenazine, pimozide, pipamperone, prochlorperazine, setoperone, spiperone, spiramide, thioridazine, thiothixene, trifluoperazine)
Volinanserin
Xylamidine
Yohimbine
Unknown/unsorted: Ergolines (e.g., dihydroergotamine, nicergoline)
5-HT2B
Agonists: 4-Methylaminorex
Aminorex
Amphetamines (e.g., chlorphentermine, cloforex, dexfenfluramine, fenfluramine, levofenfluramine, norfenfluramine)
BW-723C86
DOx (e.g., DOB, DOC, DOI, DOM)
Ergolines (e.g., cabergoline, dihydroergocryptine, dihydroergotamine, ergotamine, methylergometrine (methylergonovine), methysergide, pergolide)
Lorcaserin
MDxx (e.g., MDA (tenamfetamine), MDMA (midomafetamine), MDOH, [MMDA (drug)
Antagonists: Agomelatine
Atypical antipsychotics (e.g., amisulpride, aripiprazole, asenapine, brexpiprazole, cariprazine, clozapine, N-desalkylquetiapine (norquetiapine), N-desmethylclozapine (norclozapine), olanzapine, pipamperone, quetiapine, risperidone, ziprasidone)
Cyproheptadine
EGIS-7625
Ergolines (e.g., amesergide, bromocriptine, lisuride, LY-53857, LY-272015, mesulergine)
Ketanserin
LY-393558
mCPP
Metadoxine
Metitepine (methiothepin)
Pirenperone
Pizotifen
Propranolol
PRX-08066
Rauwolscine
Ritanserin
RS-127445
Sarpogrelate
SB-200646
SB-204741
SB-206553
SB-215505
SB-221284
SB-228357
SDZ SER-082
Tegaserod
Tetracyclic antidepressants (e.g., amoxapine, mianserin, mirtazapine)
Trazodone
Typical antipsychotics (e.g., chlorpromazine)
TIK-301
Yohimbine
Unknown/unsorted: Ergolines (e.g., ergometrine (ergonovine))
5-HT2C
Agonists: 2Cs (e.g., 2C-B, 2C-E, 2C-I, 2C-T-2, 2C-T-7, 2C-T-21)
5-Methoxytryptamines (5-MeO-DET, 5-MeO-DiPT, 5-MeO-DMT, 5-MeO-DPT, 5-MT)
α-Alkyltryptamines (e.g., 5-Cl-αMT, 5-Fl-αMT, 5-MeO-αET, 5-MeO-αMT, α-Me-5-HT, αET, αMT)
A-372159
AL-38022A
Alstonine
CP-809101
Dimemebfe
DOx (e.g., DOB, DOC, DOI, DOM)
Ergolines (e.g., ALD-52, cabergoline, dihydroergotamine, ergine (LSA), ergotamine, lisuride, LA-SS-Az, LSB, LSD, LSD-Pip, LSH, LSP, pergolide)
Flumexadol
Lorcaserin
MDxx (e.g., MDA (tenamfetamine), MDMA (midomafetamine), MDOH, MMDA)
MK-212
Org 12962
Org 37684
Oxaflozane
PHA-57378
Phenethylamines (e.g., lophophine, mescaline)
Piperazines (e.g., aripiprazole, BZP, mCPP, quipazine, TFMPP)
PNU-22394
PNU-181731
Ro60-0175
Ro60-0213
Serotonin (5-HT)
Tryptamines (e.g., 5-BT, 5-CT, bufotenin, DET, DiPT, DMT, DPT, psilocin, psilocybin, tryptamine)
Vabicaserin
WAY-629
WAY-161503
YM-348
Antagonists: Adatanserin
Agomelatine
Atypical antipsychotics (e.g., asenapine, clorotepine, clozapine, fluperlapine, iloperidone, melperone, olanzapine, paliperidone, quetiapine, risperidone, sertindole, ziprasidone, zotepine)
Captodiame
CEPC
Cinanserin
Cyproheptadine
Deramciclane
Desmetramadol
Dotarizine
Eltoprazine
Ergolines (e.g., amesergide, bromocriptine, LY-53857, LY-215840, mesulergine, metergoline, methysergide, sergolexole)
Etoperidone
Fluoxetine
FR-260010
Irindalone
Ketanserin
Ketotifen
Latrepirdine (dimebolin)
Medifoxamine
Metitepine (methiothepin)
Nefazodone
Pirenperone
Pizotifen
Propranolol
Ritanserin
RS-102221
S-14671
SB-200646
SB-206553
SB-221284
SB-228357
SB-242084
SB-243213
SDZ SER-082
Tedatioxetine
Tetracyclic antidepressants (e.g., amoxapine, aptazapine, esmirtazapine, maprotiline, mianserin, mirtazapine)
TIK-301
Tramadol
Trazodone
Tricyclic antidepressants (e.g., amitriptyline, nortriptyline)
Typical antipsychotics (e.g., chlorpromazine, loxapine, pimozide, pipamperone, thioridazine)
Xylamidine
Unknown/unsorted: Efavirenz
Ergolines (e.g., ergometrine (ergonovine), methylergometrine (methylergonovine))
5-HT3–7
5-HT3
Agonists: Alcohols (e.g., butanol, ethanol (alcohol), trichloroethanol)
m-CPBG
Phenylbiguanide
Piperazines (e.g., BZP, mCPP, quipazine)
RS-56812
Serotonin (5-HT)
SR-57227
SR-57227A
Tryptamines (e.g., 2-Me-5-HT, 5-CT, bufotenidine (5-HTQ))
Volatiles/gases (e.g., halothane, isoflurane, toluene, trichloroethane)
YM-31636
Antagonists: Alosetron
AS-8112
Atypical antipsychotics (e.g., clozapine, olanzapine, quetiapine)
Azasetron
Batanopride
Bemesetron (MDL-72222)
Bupropion
Cilansetron
CSP-2503
Dazopride
Dolasetron
Galanolactone
Granisetron
Hydroxybupropion
ICS-205930
Lerisetron
Memantine
Ondansetron
Palonosetron
Ramosetron
Renzapride
Ricasetron
Tedatioxetine
Tetracyclic antidepressants (e.g., amoxapine, mianserin, mirtazapine)
Thujone
Tropanserin
Tropisetron
Typical antipsychotics (e.g., loxapine)
Volatiles/gases (e.g., nitrous oxide, sevoflurane, xenon)
Vortioxetine
Zacopride
Zatosetron
Unknown/unsorted: LY-53857
Piperazines (e.g., naphthylpiperazine)
5-HT4
Agonists: 5-MT
BIMU8
Capeserod
Cinitapride
Cisapride
CJ-033466
Dazopride
Metoclopramide
Minesapride
Mosapride
Prucalopride
PRX-03140
Renzapride
RS-67333
RS-67506
Serotonin (5-HT)
Tegaserod
Velusetrag
Zacopride
Antagonists: GR-113808
GR-125487
L-Lysine
Piboserod
RS-39604
RS-67532
SB-203186
SB-204070
5-HT5A
Agonists: Ergolines (e.g., 2-Br-LSD (BOL-148), ergotamine, LSD)
Serotonin (5-HT)
Tryptamines (e.g., 5-CT)
Valerenic Acid
Antagonists: Asenapine
Latrepirdine (dimebolin)
Metitepine (methiothepin)
Ritanserin
SB-699551
Unknown/unsorted: Ergolines (e.g., metergoline, methysergide)
Piperazines (e.g., naphthylpiperazine)
5-HT6
Agonists: Ergolines (e.g., dihydroergocryptine, dihydroergotamine, ergotamine, lisuride, LSD, mesulergine, metergoline, methysergide)
Serotonin (5-HT)
Tryptamines (e.g., 2-Me-5-HT, 5-BT, 5-CT, 5-MT, Bufotenin, E-6801, E-6837, EMD-386088, EMDT, LY-586713, N-Me-5-HT, tryptamine)
WAY-181187
WAY-208466
Antagonists: ABT-354
Atypical antipsychotics (e.g., aripiprazole, asenapine, clorotepine, clozapine, fluperlapine, iloperidone, olanzapine, tiospirone)
AVN-101
AVN-211
AVN-322
AVN-397
BGC20-760
BVT-5182
BVT-74316
Cerlapirdine
EGIS-12233
GW-742457
Idalopirdine
Ketanserin
Landipirdine
Latrepirdine (dimebolin)
Metitepine (methiothepin)
MS-245
PRX-07034
Ritanserin
Ro 04-6790
Ro 63-0563
SB-258585
SB-271046
SB-357134
SB-399885
SB-742457
Tetracyclic antidepressants (e.g., amoxapine, mianserin)
Tricyclic antidepressants (e.g., amitriptyline, clomipramine, doxepin, nortriptyline)
Typical antipsychotics (e.g., chlorpromazine, loxapine)
Unknown/unsorted: Ergolines (e.g., 2-Br-LSD (BOL-148), bromocriptine, lergotrile, pergolide)
Piperazines (e.g., naphthylpiperazine)
5-HT7
Agonists: 8-OH-DPAT
AS-19
Bifeprunox
E-55888
Ergolines (e.g., LSD)
LP-12
LP-44
RU-24969
Sarizotan
Serotonin (5-HT)
Triptans (e.g., frovatriptan)
Tryptamines (e.g., 5-CT, 5-MT, bufotenin, N-Me-5-HT)
Antagonists: Atypical antipsychotics (e.g., amisulpride, aripiprazole, asenapine, brexpiprazole, clorotepine, clozapine, fluperlapine, olanzapine, risperidone, sertindole, tiospirone, ziprasidone, zotepine)
Butaclamol
DR-4485
EGIS-12233
Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, dihydroergotamine, ergotamine, LY-53857, LY-215840, mesulergine, metergoline, methysergide, sergolexole)
JNJ-18038683
Ketanserin
LY-215840
Metitepine (methiothepin)
Ritanserin
SB-258719
SB-258741
SB-269970
SB-656104
SB-656104A
SB-691673
SLV-313
SLV-314
Spiperone
SSR-181507
Tetracyclic antidepressants (e.g., amoxapine, maprotiline, mianserin, mirtazapine)
Tricyclic antidepressants (e.g., amitriptyline, clomipramine, imipramine)
Typical antipsychotics (e.g., acetophenazine, chlorpromazine, chlorprothixene, fluphenazine, loxapine, pimozide)
Vortioxetine
Unknown/unsorted: Ergolines (e.g., lisuride, pergolide)
Piperazines (e.g., naphthylpiperazine)
See also: Receptor/signaling modulators
Adrenergics
Dopaminergics
Melatonergics
Monoamine reuptake inhibitors and releasing agents
Monoamine metabolism modulators
Monoamine neurotoxins
[show]
v
t
e
Human trace amine-associated receptor ligands
TAAR1
Agonists
Endogenous†
Classical monoamine neurotransmitters
Dopamine
Histamine
Norepinephrine
Serotonin
Trace amines
3-Iodothyronamine
3-Methoxytyramine
N-Methylphenethylamine
N-Methyltyramine
m-Octopamine
p-Octopamine
Phenethylamine
Phenylethanolamine
Synephrine
Tryptamine
m-Tyramine
p-Tyramine
Synthetic‡
Amphetamine
DOB
DOET
4-Hydroxyamphetamine
Isoprenaline
MDA (tenamfetamine)
MDMA (midomafetamine)
2-Methylphenethylamine
3-Methylphenethylamine
4-Methylphenethylamine
β-Methylphenethylamine
Methamphetamine
3-MMA
Norfenfluramine
Phentermine
o-PIT
Propylhexedrine
RO5166017
N,N-Dimethylphenethylamine
Neutral antagonists
Inverse agonists
EPPTB (RO5212773)
TAAR2
Agonists‡
3-Iodothyronamine
Phenethylamine
Tyramine
Neutral antagonists
TAAR5
Agonists‡
Dimethylethylamine
Trimethylamine
Neutral antagonists
Inverse agonists‡
3-Iodothyronamine
†References for all endogenous human TAAR1 ligands are provided at List of trace amines

‡References for synthetic TAAR1 agonists can be found at TAAR1 or in the associated compound articles. For TAAR2 and TAAR5 agonists and inverse agonists, see TAAR for references.

See also: Receptor/signaling modulators
[show]
v
t
e
Tryptamines
1-Methylpsilocin
2-Methyl-5-HT
4,5-DHP-DMT
4,5-MDO-DMT
4,5-MDO-DiPT
4-AcO-DALT
4-AcO-DET
4-AcO-DMT
4-AcO-DiPT
4-AcO-NMT
4-AcO-MET
4-AcO-DPT
4-AcO-MiPT
4-HO-DALT
4-HO-DET
4-HO-DiPT
4-HO-DSBT
4-HO-MET
4-HO-MiPT
4-HO-NMT
4-HO-αMT
4-Me-αET
4-Me-αMT
4-MeO-DiPT
4-MeO-DMT
5-BT
5-Bromo-DMT
5-CT
5-Chloro-αMT
5-Ethoxy-αMT
5-Fluoro-αMT
5-HO-αMT
5-HO-DiPT
5-HTP
5-Ethoxy-DMT
5-Ethyl-DMT
5-Fluoro-DMT
5-Methyl-DMT
5-Methoxytryptamine
5-MeO-7,N,N-TMT
5-Methyl-αET
5-MeO-αET
5-MeO-αMT
5-MeO-DALT
5-MeO-DET
5-MeO-DiPT
5-MeO-DMT
5-MeO-DPT
5-MeO-EiPT
5-MeO-EPT
5-MeO-MALT
5-MeO-MiPT
5-MeO-NBpBrT
5,7-Dihydroxytryptamine
5-(Nonyloxy)tryptamine
6-Fluoro-αMT
6-Hydroxymelatonin
7-Methyl-αET
7-Methyl-DMT
Acetryptine
Aeruginascin
αET
AL-37350A
αMT
BW-723C86
Baeocystin
Bufotenidine
Bufotenin (5-HO-DMT)
Convolutindole A
DALT
Desformylflustrabromine
DET
DiPT
DMT
DPT
Ethocybin
EiPT
EMDT
EPT
FGIN-127
FGIN-143
HIOC
Ibogaine
Indorenate
Iprocin
Lespedamine
Luzindole
MET
MiPT
MPT
Miprocin
Melatonin
MS-245
NAS
N-Feruloylserotonin
NMT
Norbaeocystin
Normelatonin
O-4310
Oxypertine
Plakohypaphorine
PiPT
Psilocin (4-HO-DMT)
Psilocybin (4-PO-DMT)
Rizatriptan
Serotonin
ST-1936
Sumatriptan
Tryptamine
Tryptophan
Yohimbine
Yuremamine
Zolmitriptan
Authority control
GND: 4054614-7
NDL: 00570824
Chemistry portal
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Serotonin (disambiguation)

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Skeletal formula of serotonin

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G-protein-coupled receptors

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Second messenger

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Tricyclic antidepressants

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values: In this drawing of the brain, the serotonergic system is red and the mesolimbic dopamine pathway is blue. There is one collection of serotonergic neurons in the upper brainstem that sends axons upwards to the whole cerebrum, and one collection next to the cerebellum that sends axons downward to the spinal cord. Slightly forward the upper serotonergic neurons is the ventral tegmental area (VTA), which contains dopaminergic neurons. These neurons' axons then connect to the nucleus accumbens, hippocampus and the frontal cortex. Over the VTA is another collection of dopaminergic cells, the substansia nigra, which send axons to the striatum.

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Neurotransmitter system

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Presynaptic terminal

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Incentive salience

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Ventromedial nucleus

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5-HT antagonist

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Psychedelic mushroom

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5HT2C receptor

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Selective and non-selective

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