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Template:Chembox InChI
CAS number 50-67-9
PubChem 5202
MeSH Serotonin
SMILES NCCc1c[nH]c2ccc(O)cc12
Molecular formula </sub>C10H12N2O
Molar mass 176.215
materials in their standard state
(at 25 °C, 100 kPa)

Infobox disclaimer and references



File:5-HT numbered.svg

In the central nervous system, serotonin plays an important role as a neurotransmitter in the modulation of anger, aggression, body temperature, mood, sleep, human sexuality, appetite, and metabolism, as well as stimulating vomiting.[1]


Levels of serotonin in the brain show association with aggression [4], and a mutation in the gene which codes for the 5-HT2A receptor may double the risk of suicide for those with that genotype.[5]


In addition, serotonin is also a peripheral signal mediator. It is found extensively in the human gastrointestinal tract as about 80-90% of the body's total serotonin is found in the enterochromaffin cells in the gut.[7][8] In the blood, the major storage site is platelets, which collect serotonin for use in mediating post-injury vasoconstriction.[9]

Recent research suggests that serotonin plays an important role in liver regeneration and acts as a mitogen (induces cell division) throughout the body. Recent research also suggests that intestinal serotonin may inhibit bone formation. [1] [10]

Serotonin and SIDS

Defective signalling of serotonin in the brain may be the root cause of sudden infant death syndrome (SIDS), Italian researchers have found. Scientists from the European Molecular Biology Laboratory in Monterotondo, Italy,[11] genetically modified lab mice to produce low levels of the brain signaling protein serotonin. The results showed the mice suffered drops in heart rate and other symptoms of SIDS, and many of the animals died at an early age.


Serotonin and psychology

Serotonin, or 5-hydroxytryptamine (5-HT), has been implicated in almost every conceivable physiologic or behavioral function—affect, aggression, appetite, cognition, emesis,endocrine function, gastrointestinal function, motor function, neurotrophism, perception, sensory function, sex,sleep, and vascular function (1).Moreover, most drugs that are currently used for the treatment of psychiatric disorders(e.g., depression, mania, schizophrenia, autism, obsessivecompulsive disorder, anxiety disorders) are thought to act, at least partially, through serotoninergic mechanisms .How is it possible for 5-HT to be involved in so many different processes? One answer lies in the anatomy of the serotoninergic system, in which 5-HT cell bodies clustered in the brainstem raphe nuclei are positioned through their vast projections to influence all regions of the neuraxis.Another answer lies in the molecular diversity and differential cellular distribution of the many 5-HT receptor subtypes that are expressed in brain and other tissues.<Blockquote/>


As with all neurotransmitters, the effects of 5-HT on the human mood and state of mind, and its role in consciousness, are very difficult to ascertain.

Gross anatomy

The neurons of the raphe nuclei are the principal source of 5-HT release in the brain.[13] The raphe nuclei are neurons grouped into about nine pairs and distributed along the entire length of the brainstem, centered around the reticular formation. [14]



Thus, activation of this serotonin system has effects on large areas of the brain, which explains the effects of therapeutic modulation of it.


5-HT is thought to be released from serotonergic varicosities into the extra neuronal space, in other words from swellings (varicosities) along the axon, rather than from synaptic terminal buttons (in the manner of classical neurotransmission). From here it is free to diffuse over a relatively large region of space (>20µm) and activate 5-HT receptors located on the dendrites, cell bodies and presynaptic terminals of adjacent neurons.

Main article: 5-HT receptor


Genetic factors

Genetic variations in alleles which code for serotonin receptors are now known to have a significant impact on the likelihood of the appearance of certain psychological disorders and problems. For instance, a mutation in the allele which codes for the 5-HT2A receptor appears to double the risk of suicide for those with that genotype. [2]. However, evidence for this has yet to be replicated satisfactorily, and doubts over the validity of this finding have been raised. It is very unlikely that one individual gene could be responsible for increased suicides. It is more probable that a number of genes combine with environmental factors to affect behaviour in this way.



Other functions


=Brain development

Recent experimental data support the role of serotonin in modulating brain development, so that a dysfunction in serotonergic activity in early life could lead to long lasting structural and functional alterations.


If neurons of the brainstem that make serotonin — serotonergic neurons — are abnormal in infants, there is a risk of sudden infant death syndrome (SIDS).[16][17] Low levels of serotonin may also be associated with intense religious experiences.[18]

It has also been discovered that serial killers consistently have low levels of serotonin. This is possibly a result of the aggressive and angry behaviors also associated with low levels of serotonin).

Recent research conducted at Rockefeller University shows that in both patients who suffer from depression and in mice that model that disease, levels of the p11 protein are decreased. This protein is related to serotonin transmission within the brain.[19]


File:Serotonin biosynthesis.svg




Serotonergic drugs

Several classes of drugs target the 5-HT system including some antidepressants, antipsychotics, anxiolytics, antiemetics, and antimigraine drugs as well as the psychoactive drugs psychedelic drugs and empathogens.

Psychoactive drugs




Some drugs inhibit this re-uptake of serotonin, again making it stay in the synapse longer. The tricyclic antidepressants (TCAs) inhibit the re-uptake of both serotonin and norepinephrine. The newer selective serotonin re-uptake inhibitors (SSRIs) have fewer (though still numerous) side-effects and fewer interactions with other drugs.

Like many centrally active drugs, prolonged use of SSRIs may not be effective for increasing levels of serotonin as homeostasis may reverse the effects of SSRIs via negative feedback, tolerance or downregulation.



Serotonin syndrome

Extremely high levels of serotonin can have toxic and potentially fatal effects, causing a condition known as serotonin syndrome. In practice, such toxic levels are essentially impossible to reach through an overdose of a single anti-depressant drug, but require a combination of serotonergic agents, such as an SSRI with an MAOI.[20] The intensity of the symptoms of serotonin syndrome vary over a wide spectrum, and the milder forms are seen even at non-toxic levels.[21] For example, recreational doses of MDMA (ecstasy) will generally cause such symptoms but only rarely lead to true toxicity.

Chronic diseases resulting from serotonin 5-HT2B overstimulation

Main article: Cardiac fibrosis



Serotonergic agonist drugs in overdose in experimental animals not only cause acute (and sometimes fatal) pulmonary hypertension, but there is epidemiologic evidence that chronic use of certain of these drugs produce a chronic pulmonary hypertensive syndrome in humans, also. Some serotinergic agonist drugs also cause fibrosis anywhere in the body, particularly the syndrome of retroperitoneal fibrosis, as well as right-sided cardiac valve fibrosis.

In the past, three groups of serotonergic drugs have been epidemiolgically linked with these syndromes. They are the serotonergic vasoconstrictive anti-migraine drugs (ergotamine and methysergide), 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 specific lisuride). A number of these drugs have recently been withdrawn from the market after groups taking them showed a statistical increase of one or more off the side effects described.


In unicellular organisms

Serotonin is used by a variety of single-cell organisms for various purposes. Selective serotonin re-uptake inhibitors (SSRIs) have been found to be toxic to algae.[22] The gastrointestinal parasite Entamoeba histolytica secretes serotonin, causing a sustained secretory diarrhea in some patients.[23][24] Patients infected with Entamoeba histolytica have been found to have highly elevated serum serotonin levels which returned to normal following resolution of the infection.[25]Entamoeba histolytica also responds to the presence of serotonin by becoming more virulent.[26]

In animals

Serotonin as a neurotransmitter is found in all animals, including insects. Several toad venoms, as well as that of the Brazilian Wandering Spider and stingray, contain serotonin and related tryptamines.



See also

References & Bibliography

Key texts



  • Aghajanian, GK, Sanders-Bush, E. Serotonin. Fulltext
  • Svenningsson P, Chergui K, Rachleff I, Flajolet M, Zhang X, Yacoubi ME, Vaugeois JM, Nomikos GG, Greengard P. Alterations in 5-HT1B receptor function by p11 in depression-like states. Science 2006;311(5757):77–80. PMID 16400147

Additional material



  • Burrell, B.D. & Sahley, C.L. (1999). Serotonin Depletion Does Not Prevent Intrinsic Sensitization in the Leech. Learning & Memory, 6, 509 - 520. Full text

External links

Tryptamines edit


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