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Serotonin

Also called 5-Hydroxytryptamine, Thrombotonin, Thrombocytin

Original Wikipedia articleen.wikipedia.org/wiki/Serotonin revision used (24 October 2026)

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Enzymes that break it down: monoamine oxidase (MAO). Wikipedia’s drug infobox says: “MAO, AANAT” (revision 1378486640).

Dosage

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Duration

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Mixing

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Risks and toxicity

Serotonin syndrome

Extremely high levels of serotonin can cause a condition known as serotonin syndrome, which possess both toxic and potentially life threatening effects. PW

Serotonin syndrome, also known as serotonin toxicity, is not known to occur naturally without the introduction of a pharmaceutical or supplemental agent. However, serotonin syndrome is known to develop from naturally occurring compounds such as St. John's Wort, a treatment for depression, due to its similarities to already existing antidepressants. Excess amounts of serotonin in the brain is primarily caused by the concurrent use of two or more serotonin acting drugs.[16] PW

An example that may result in serotonin syndrome would include taking two antidepressants in combination such as Escitalopram (Lexapro) with Duloxetine (Cymbalta), since both drugs act on some of the same receptors they may cause serotonin syndrome. PW

Another example would be taking a prescription antidepressant in combination with an over the counter cough suppressant such as dextromethorphan.The number of possibly dangerous combinations are numerous. If you are currently taking an antidepressant or are considering taking a new substance, ensure that no dangerous interactions exist.[17][18] PW

Symptoms can start showing within hours and can include: increased or irregular heart rate, tremors, low-grade fever to fevers at or over 41°C (105.8°F), sweating, anxiety, hyperthermia, shivering, high blood pressure, restlessness, dilation of the pupils, overactive or over responsive reflexes, agitation, confusion, death of muscle fibers, clotting of small blood vessels, increase in body acidity, delirium, renal (kidney) failure, coma and rarely death.[19] PW

Symptoms in minor cases may resolves within days, moderate cases may resolve within weeks, and in severe cases permanent damage or death may occur. PW

Testing

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Effects

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Overview

Serotonin (also known as 5-hydroxytryptamine, or 5-HT), is a naturally occuring chemical found in humans, animals, and plants alike. PW

Serotonin (/ˌsɛrəˈtoʊnᵻn,_ˌsɪərə-/), also known as 5-hydroxytryptamine (5-HT), is a monoamine neurotransmitter with a wide range of functions in both the central nervous system (CNS) and also peripheral tissues. It is involved in mood, cognition, reward, learning, memory, and physiological processes such as vomiting and vasoconstriction. In the CNS, serotonin regulates mood, appetite, and sleep.[1][2][3] WP⚠ The source has a footnote here that is not shown.⚠ Part of this sentence could not be copied from the source. Open the source to read it in full.⚠ Wikipedia itself has flagged this text: unreliable medical source?.

Most of the body's serotonin—about 90%—is synthesized in the gastrointestinal tract by enterochromaffin cells, where it regulates intestinal movements. It is also produced in smaller amounts in the brainstem's raphe nuclei, the skin's Merkel cells, pulmonary neuroendocrine cells, and taste receptor cells of the tongue. Once secreted, serotonin is taken up by platelets in the blood, which release it during clotting to promote vasoconstriction and platelet aggregation. Around 8% of the body's serotonin is stored in platelets, and 1–2% is found in the CNS.[4–8] WP

Serotonin acts as both a vasoconstrictor and vasodilator depending on concentration and context, influencing hemostasis and blood pressure regulation. It plays a role in stimulating myenteric neurons and enhancing gastrointestinal motility through uptake and release cycles in platelets and surrounding tissue. Biochemically, serotonin is an indoleamine synthesized from tryptophan and metabolized primarily in the liver to 5-hydroxyindoleacetic acid (5-HIAA).[9][10] WP

Serotonin is targeted by several classes of antidepressants, including selective serotonin reuptake inhibitors (SSRIs) and serotonin–norepinephrine reuptake inhibitors (SNRIs), which block reabsorption in the synapse to elevate its levels. It is found in nearly all bilateral animals, including insects, spiders and worms, and also occurs in fungi and plants. In plants and insect venom, it serves a defensive function by inducing pain. Serotonin released by pathogenic amoebae may cause diarrhea in the human gut, while its presence in seeds and fruits is thought to stimulate digestion and facilitate seed dispersal.[11–15] WP⚠ Wikipedia itself has flagged this text: failed verification.

History

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Pharmacology

Pharmacology

Several classes of drugs target the serotonin system, including some antidepressants, anxiolytics, antipsychotics, analgesics, antimigraine drugs, oxytocics, antiemetics, appetite suppressants, and anticonvulsants, as well as psychedelics and entactogens. WP

Mechanism of action

At rest, serotonin is stored within the vesicles of presynaptic neurons. When stimulated by nerve impulses, serotonin is released as a neurotransmitter into the synapse, reversibly binding to the postsynaptic receptor to induce a nerve impulse on the postsynaptic neuron. Serotonin can also bind to auto-receptors on the presynaptic neuron to regulate the synthesis and release of serotonin. Normally serotonin is taken back into the presynaptic neuron to stop its action, then reused or broken down by monoamine oxidase.[26] WP

Antidepressants

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.[27] WP

Certain SSRI medications have been shown to lower serotonin levels below the baseline after chronic use, despite initial increases. 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. The 5-HTTLPR polymorphism (l/l) causing more serotonin transporters to be formed is also found to be more resilient against depression and anxiety.[28–31] WP

Besides their use in treating depression and anxiety, certain serotonergic antidepressants are also approved and used to treat fibromyalgia, neuropathic pain, and chronic fatigue syndrome.[32][33] WP

Anxiolytics

Azapirone anxiolytics like buspirone and tandospirone act as serotonin 5-HT1A receptor agonists.[34][35] WP

Antipsychotics

Many antipsychotics bind to and modulate serotonin receptors, including the serotonin 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C, 5-HT₆, and 5-HT₇ receptors, among others. Activation of serotonin 5-HT1A receptors and blockade of serotonin 5-HT2A receptors may contribute to the therapeutic antipsychotic effects of these agents, whereas antagonism of serotonin 5-HT2C receptors has been especially implicated in side effects of antipsychotics.[36][37] WP

Antimigraine agents

Antimigraine agents such as the triptans like sumatriptan act as agonists of the serotonin 5-HT1B, 5-HT1D, and/or 5-HT1F receptors. Earlier antimigraine agents were the ergoline derivatives and ergot-related drugs such as ergotamine, dihydroergotamine, and methysergide, which act as non-selective serotonin receptor agonists.[38–41] WP

Oxytocics

Certain lysergamides like ergometrine and methylergometrine are used clinically as oxytocic agents. The oxytocic effects of these drugs are thought to most likely be mediated by agonism of serotonin 5-HT₂ receptors in uterine smooth muscle tissue.[42][43] WP

Antiemetics

Some serotonin 5-HT₃ receptor 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.[44][45] WP

Appetite suppressants

Some serotonin releasing agents, serotonin reuptake inhibitors, and/or serotonin 5-HT2C receptor agonists, such as fenfluramine, dexfenfluramine, chlorphentermine, sibutramine, and lorcaserin, have been approved and used as appetite suppressants for purposes of weight loss in the treatment of overweightness or obesity. Several of the preceding agents have been withdrawn from the market due to toxicity, such as cardiac fibrosis or pulmonary hypertension.[46–50] WP

Anticonvulsants

Although it was previously withdrawn from the market as an appetite suppressant, fenfluramine was reintroduced as an anticonvulsant for treatment of seizures in certain rare forms of epilepsy like Dravet syndrome and Lennox–Gastaut syndrome. Selective serotonin 5-HT2C receptor agonists, like lorcaserin, bexicaserin, and BMB-101, are also being developed for this use.[51–54] WP

Psychedelics

Serotonergic psychedelics, including drugs like psilocybin (found in psilocybin mushrooms), dimethyltryptamine (DMT) (found in ayahuasca), lysergic acid diethylamide (LSD), mescaline (found in peyote cactus), and 5-MeO-DMT (found in Anadenanthera trees and the Bufo alvarius toad), are non-selective agonists of the serotonin receptors and mediate their hallucinogenic effects specifically by activation of the serotonin 5-HT2A receptor. This is evidenced by the fact that serotonin 5-HT2A receptor antagonists and so-called "trip killers" like ketanserin block the hallucinogenic effects of serotonergic psychedelics in humans, among many other findings. Some serotonergic psychedelics, like psilocin, DMT, and 5-MeO-DMT, are substituted tryptamines and are very similar in chemical structure to serotonin.[55–58] WP

Serotonin itself, despite acting as a serotonin 5-HT2A receptor agonist, is thought to be non-hallucinogenic. The hallucinogenic effects of serotonergic psychedelics are believed to be related to activation of serotonin 5-HT2A receptors expressed in a population of cortical neurons in the medial prefrontal cortex (mPFC). These serotonin 5-HT2A receptors, unlike most serotonin and related receptors, are expressed intracellularly. In addition, the neurons containing them lack expression of the serotonin transporter (SERT), which normally transports serotonin from the extracellular space to the intracellular space within neurons. Serotonin itself is too hydrophilic to enter serotonergic neurons without the SERT, and hence these serotonin 5-HT2A receptors are inaccessible to serotonin. Conversely, serotonergic psychedelics are more lipophilic than serotonin and readily enter these neurons. In addition to explaining why serotonin does not show psychedelic effects, these findings may explain why drugs that increase serotonin levels, like selective serotonin reuptake inhibitors (SSRIs) and various other types of serotonergic agents, do not produce psychedelic effects. Artificial expression of the SERT in these medial prefrontal cortex neurons resulted in the serotonin releasing agent para-chloroamphetamine (PCA), which did not otherwise show psychedelic-like effects, being able to produce psychedelic-like effects in animals.[59][60] WP

Although serotonin itself is thought to be non-hallucinogenic, administration of very high doses of a serotonin precursor, like tryptophan or 5-hydroxytryptophan (5-HTP), or intracerebroventricular injection of high doses of serotonin directly into the brain, can produce psychedelic-like effects in animals. These psychedelic-like effects can be abolished by indolethylamine N-methyltransferase (INMT) inhibitors, which block conversion of serotonin and other endogenous tryptamines into N-methylated tryptamines, including N-methylserotonin (NMS; norbufotenin), bufotenin (5-hydroxy-N,N-dimethyltryptamine; 5-HO-DMT), N-methyltryptamine (NMT), and N,N-dimethyltryptamine (DMT). These N-methyltryptamines are much more lipophilic than serotonin and, in contrast, are able to diffuse into serotonergic neurons and activate intracellular serotonin 5-HT2A receptors. Another metabolite of serotonin with possible psychedelic-like effects in animals is 5-methoxytryptamine (5-MT).[59–67] WP

DMT is a naturally occurring endogenous compound in the body. In relation to the fact that serotonin itself is unable to activate intracellular serotonin 5-HT2A receptors, it is possible that DMT might be the endogenous ligand of these receptors rather than serotonin.[59][60][68][69][70] WP

Entactogens

The entactogen MDMA is a serotonin releasing agent and, while it also possesses other actions such as concomitant release of norepinephrine and dopamine and weak direct agonism of the serotonin 5-HT₂ receptors, its serotonin release plays a key role in its unique entactogenic effects. Entactogens like MDMA should be distinguished from other drugs such as stimulants like amphetamine and psychedelics like LSD, although MDMA itself also has some characteristics of both of these types of agents. Coadministration of selective serotonin reuptake inhibitors (SSRIs), which block the serotonin transporter (SERT) and prevent MDMA from inducing serotonin release, markedly reduce the subjective effects of MDMA, demonstrating the key role of serotonin in the effects of the drug. Serotonin releasing agents like MDMA achieve much greater increases in serotonin levels than SSRIs and have far more robust of subjective effects. Besides MDMA, many other entactogens also exist and are known.[71–79] WP

Serotonin syndrome

Extremely high levels of serotonin or activation of certain serotonin receptors 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 a MAOI, which may occur in therapeutic doses. However, serotonin syndrome can occur with overdose of certain serotonin receptor agonists, like the NBOMe series of serotonergic psychedelics.[80–84] WP

The intensity of the symptoms of serotonin syndrome vary over a wide spectrum, and the milder forms are seen even at nontoxic levels. It is estimated that 14% of patients experiencing serotonin syndrome overdose on SSRIs; while the fatality rate is between 2% and 12%.[80][85][86][87] WP

Cardiac fibrosis and other fibroses

Some serotonergic agonist drugs cause fibrosis anywhere in the body, particularly the syndrome of retroperitoneal fibrosis, as well as cardiac valve fibrosis.[88] WP

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), 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.[88][89] WP

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.[90] WP

Two independent studies published in The New England Journal of Medicine in January 2007 implicated pergolide, along with cabergoline, in causing valvular heart disease. As a result of this, the FDA removed pergolide from the United States market in March 2007. (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).[91–94] WP

Receptor binding · Wikipedia

Binding profile of serotonin

col1col2col3
5-HT1A3.17Memory (agonists ↓); learning (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 ↓) WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT1B4.32Vasoconstriction (agonists ↑); aggression (agonists ↓); bone mass (↓). Serotonin autoreceptor. WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT1D5.03Vasoconstriction (agonists ↑) WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT1E7.53 WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT1F10 WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT2A11.55Psychedelia (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 ↑); dopamine in the prefrontal cortex (agonists ↑); urinary bladder contractions (agonists ↑)[20][21] WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT2B8.71Cardiovascular functioning (agonists increase risk of pulmonary hypertension), empathy (via von Economo neurons)[22] WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT2C5.02Dopamine release into the mesocorticolimbic pathway (agonists ↓); acetylcholine release in the prefrontal cortex (agonists ↑); dopaminergic and noradrenergic activity in the frontal cortex (antagonists ↑); appetite (agonists ↓); antipsychotic effects (agonists ↑); antidepressant effects (agonists & antagonists ↑)[23] WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT₃593Emesis (agonists ↑); anxiolysis (antagonists ↑). WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT₄125.89Movement of food across the GI tract (agonists ↑); memory & learning (agonists ↑); antidepressant effects (agonists ↑). Signalling via Gαs activation of adenylyl cyclase. WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT5A251.2Memory consolidation. Signals via Gi/o inhibition of adenylyl cyclase.[24] WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT₆98.41Cognition (antagonists ↑); antidepressant effects (agonists & antagonists ↑); anxiogenic effects (antagonists ↑). Gₛ signalling via activating adenylyl cyclase.[25] WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.
5-HT₇8.11Cognition (antagonists ↑); antidepressant effects (antagonists ↑). Acts by Gₛ signalling via activating adenylyl cyclase. WP⚠ This row of the source table has a different number of cells than its headings, so columns may not line up.

Chemistry

Formula
C10H12N2O PC
CAS number
50-67-9 PC
Molar mass (g/mol)
176.21 PC
IUPAC name (computed by PubChem)
3-(2-aminoethyl)-1H-indol-5-ol PC
SMILES
C1=CC2=C(C=C1O)C(=CN2)CCN PC
InChIKey
QZAYGJVTTNCVMB-UHFFFAOYSA-N PC
PubChem CID
5202

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References

  1. Journal / agency Young SN. How to increase serotonin in the human brain without drugs. Journal of Psychiatry & Neuroscience. November 2007. doi:10.1139/jpn.0738 · PMID 18043762 · PMC2077351
  2. Journal / agency Sangare A, Dubourget R, Geoffroy H, Gallopin T, Rancillac A. Serotonin differentially modulates excitatory and inhibitory synaptic inputs to putative sleep-promoting neurons of the ventrolateral preoptic nucleus. Neuropharmacology. October 2016. doi:10.1016/j.neuropharm.2016.05.015 · PMID 27238836
  3. Journal / agency Rancillac A. Serotonin and sleep-promoting neurons. Oncotarget. November 2016. doi:10.18632/oncotarget.13419 · PMID 27861160 · PMC5346632
  4. Other Microbes Help Produce Serotonin in Gut. 2015-04-09
  5. Other King MW. Serotonin. 2020-05-18
  6. Journal / agency Berger M, Gray JA, Roth BL. The expanded biology of serotonin. Annual Review of Medicine. 2009. doi:10.1146/annurev.med.60.042307.110802 · PMID 19630576 · PMC5864293
  7. Journal / agency Schlienger RG, Meier CR. Effect of selective serotonin reuptake inhibitors on platelet activation: can they prevent acute myocardial infarction?. American Journal of Cardiovascular Drugs. 2003. doi:10.2165/00129784-200303030-00001 · PMID 14727927
  8. Other Kling A. 5-HT2A: a serotonin receptor with a possible role in joint diseases. 2013
  9. Journal / agency Vanhoutte PM. Serotonin and the vascular wall. International Journal of Cardiology. February 1987. doi:10.1016/0167-5273(87)90008-8 · PMID 3818135
  10. Journal / agency Yano JM, Yu K, Donaldson GP, Shastri GG, Ann P, Ma L, Nagler CR, Ismagilov RF, Mazmanian SK, Hsiao EY. Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Cell. April 2015. doi:10.1016/j.cell.2015.02.047 · PMID 25860609 · PMC4393509
  11. Journal / agency Huser A, Rohwedder A, Apostolopoulou AA, Widmann A, Pfitzenmaier JE, Maiolo EM, Selcho M, Pauls D, von Essen A, Gupta T, Sprecher SG, Birman S, Riemensperger T, Stocker RF, Thum AS. The serotonergic central nervous system of the Drosophila larva: anatomy and behavioral function. PLOS ONE. 2012. doi:10.1371/journal.pone.0047518 · PMID 23082175 · PMC3474743
  12. Journal / agency Ramakrishna A, Giridhar P, Ravishankar GA. Phytoserotonin: a review. Plant Signaling & Behavior. June 2011. doi:10.4161/psb.6.6.15242 · PMID 21617371 · PMC3218476
  13. Journal / agency Erspamer V. 5-Hydroxytryptamine and Related Indolealkylamines. 1966. doi:10.1007/978-3-642-85467-5_4
  14. Journal / agency McGowan K, Kane A, Asarkof N, Wicks J, Guerina V, Kellum J, Baron S, Gintzler AR, Donowitz M. Entamoeba histolytica causes intestinal secretion: role of serotonin. Science. August 1983. doi:10.1126/science.6308760 · PMID 6308760
  15. Journal / agency Feldman JM, Lee EM. Serotonin content of foods: effect on urinary excretion of 5-hydroxyindoleacetic acid. The American Journal of Clinical Nutrition. October 1985. doi:10.1093/ajcn/42.4.639 · PMID 2413754
  16. Journal / agency Lane, R., Baldwin, D. Selective Serotonin Reuptake Inhibitor-Induced Serotonin Syndrome: Review. Journal of Clinical Psychopharmacology. June 1997. doi:10.1097/00004714-199706000-00012
  17. Journal / agency Monte, A. A., Chuang, R., Bodmer, M. Dextromethorphan, chlorphenamine and serotonin toxicity: case report and systematic literature review: Dextromethorphan, chlorphenamine and serotonin toxicity. British Journal of Clinical Pharmacology. December 2010. doi:10.1111/j.1365-2125.2010.03747.x
  18. Journal / agency Schwartz, A. R., Pizon, A. F., Brooks, D. E. Dextromethorphan-induced serotonin syndrome. Clinical Toxicology. January 2008. doi:10.1080/15563650701668625
  19. Journal / agency Frank, C. Recognition and treatment of serotonin syndrome. Canadian Family Physician. 1 July 2008
  20. Journal / agency Bortolozzi A, Díaz-Mataix L, Scorza MC, Celada P, Artigas F. The activation of 5-HT receptors in prefrontal cortex enhances dopaminergic activity. Journal of Neurochemistry. December 2005. doi:10.1111/j.1471-4159.2005.03485.x · PMID 16277612
  21. Journal / agency Moro C, Edwards L, Chess-Williams R. 5-HT2A receptor enhancement of contractile activity of the porcine urothelium and lamina propria. International Journal of Urology. November 2016. doi:10.1111/iju.13172 · PMID 27531585
  22. Other code. Von Economo neuron – NeuronBank. 2025-10-03
  23. Journal / agency Millan MJ, Gobert A, Lejeune F, Dekeyne A, Newman-Tancredi A, Pasteau V, Rivet JM, Cussac D. The novel melatonin agonist agomelatine (S20098) is an antagonist at 5-hydroxytryptamine2C receptors, blockade of which enhances the activity of frontocortical dopaminergic and adrenergic pathways. The Journal of Pharmacology and Experimental Therapeutics. September 2003. doi:10.1124/jpet.103.051797 · PMID 12750432
  24. Journal / agency Gonzalez R, Chávez-Pascacio K, Meneses A. Role of 5-HT5A receptors in the consolidation of memory. Behavioural Brain Research. September 2013. doi:10.1016/j.bbr.2013.05.051 · PMID 23735322
  25. Journal / agency Nautiyal KM, Hen R. Serotonin receptors in depression: from A to B. F1000Research. 2017. doi:10.12688/f1000research.9736.1 · PMID 28232871 · PMC5302148
  26. Journal / agency Fuller RW. Pharmacology of central serotonin neurons. Annual Review of Pharmacology and Toxicology. 1980. doi:10.1146/annurev.pa.20.040180.000551 · PMID 6992697
  27. Other Goodman LS, Brunton LL, Chabner B, Knollmann BC. Goodman and Gilman's pharmacological basis of therapeutics. 2001
  28. Journal / agency Benmansour S, Cecchi M, Morilak DA, Gerhardt GA, Javors MA, Gould GG, Frazer A. Effects of chronic antidepressant treatments on serotonin transporter function, density, and mRNA level. The Journal of Neuroscience. December 1999. doi:10.1523/JNEUROSCI.19-23-10494.1999 · PMID 10575045 · PMC6782424
  29. Journal / agency Beitchman JH, Baldassarra L, Mik H, De Luca V, King N, Bender D, Ehtesham S, Kennedy JL. Serotonin transporter polymorphisms and persistent, pervasive childhood aggression. The American Journal of Psychiatry. June 2006. doi:10.1176/appi.ajp.163.6.1103 · PMID 16741214
  30. Journal / agency Pezawas L, Meyer-Lindenberg A, Drabant EM, Verchinski BA, Munoz KE, Kolachana BS, Egan MF, Mattay VS, Hariri AR, Weinberger DR. 5-HTTLPR polymorphism impacts human cingulate-amygdala interactions: a genetic susceptibility mechanism for depression. Nature Neuroscience. June 2005. doi:10.1038/nn1463 · PMID 15880108
  31. Journal / agency Schinka JA, Busch RM, Robichaux-Keene N. A meta-analysis of the association between the serotonin transporter gene polymorphism (5-HTTLPR) and trait anxiety. Molecular Psychiatry. February 2004. doi:10.1038/sj.mp.4001405 · PMID 14966478
  32. Journal / agency O'Malley PG, Jackson JL, Santoro J, Tomkins G, Balden E, Kroenke K. Antidepressant therapy for unexplained symptoms and symptom syndromes. The Journal of Family Practice. December 1999. PMID 10628579
  33. Journal / agency Welsch P, Üçeyler N, Klose P, Walitt B, Häuser W. Serotonin and noradrenaline reuptake inhibitors (SNRIs) for fibromyalgia. The Cochrane Database of Systematic Reviews. February 2018. doi:10.1002/14651858.CD010292.pub2 · PMID 29489029 · PMC5846183
  34. Journal / agency Taylor DP, Moon SL. Buspirone and related compounds as alternative anxiolytics. Neuropeptides. July 1991. doi:10.1016/0143-4179(91)90078-w · PMID 1679210
  35. Journal / agency Kishi T, Meltzer HY, Matsuda Y, Iwata N. Azapirone 5-HT1A receptor partial agonist treatment for major depressive disorder: systematic review and meta-analysis. Psychological Medicine. August 2014. doi:10.1017/S0033291713002857 · PMID 24262766
  36. Journal / agency Meltzer HY. The role of serotonin in antipsychotic drug action. Neuropsychopharmacology. August 1999. doi:10.1016/S0893-133X(99)00046-9 · PMID 10432496
  37. Journal / agency Meltzer HY. Handb Exp Pharmacol. 2012. doi:10.1007/978-3-642-25761-2_4 · PMID 23129329
  38. Journal / agency Tfelt-Hansen P, De Vries P, Saxena PR. Triptans in migraine: a comparative review of pharmacology, pharmacokinetics and efficacy. Drugs. December 2000. doi:10.2165/00003495-200060060-00003 · PMID 11152011
  39. Journal / agency Ramírez Rosas MB, Labruijere S, Villalón CM, Maassen Vandenbrink A. Activation of 5-hydroxytryptamine1B/1D/1F receptors as a mechanism of action of antimigraine drugs. Expert Opinion on Pharmacotherapy. August 2013. doi:10.1517/14656566.2013.806487 · PMID 23815106
  40. Journal / agency Saxena PR, Den Boer MO. Pharmacology of antimigraine drugs. Journal of Neurology. 1991. doi:10.1007/BF01642903 · PMID 1646288
  41. Journal / agency Whealy M, Becker WJ. Handbook of Clinical Neurology. 2024. doi:10.1016/B978-0-12-823357-3.00008-2 · PMID 38307644
  42. Journal / agency Schiff PL. Ergot and its alkaloids. American Journal of Pharmaceutical Education. October 2006. doi:10.5688/aj700598 · PMID 17149427 · PMC1637017
  43. Journal / agency Vallera C, Choi LO, Cha CM, Hong RW. Uterotonic Medications: Oxytocin, Methylergonovine, Carboprost, Misoprostol. Anesthesiology Clinics. June 2017. doi:10.1016/j.anclin.2017.01.007 · PMID 28526143
  44. Journal / agency Ho KY, Gan TJ. Pharmacology, pharmacogenetics, and clinical efficacy of 5-hydroxytryptamine type 3 receptor antagonists for postoperative nausea and vomiting. Current Opinion in Anaesthesiology. December 2006. doi:10.1097/01.aco.0000247340.61815.38 · PMID 17093363
  45. Journal / agency Seynaeve C, Verweij J, de Mulder PH. 5-HT3 receptor antagonists, a new approach in emesis: a review of ondansetron, granisetron and tropisetron. Anti-Cancer Drugs. August 1991. doi:10.1097/00001813-199108000-00003 · PMID 1665723
  46. Journal / agency Halford JC, Harrold JA, Boyland EJ, Lawton CL, Blundell JE. Serotonergic drugs: effects on appetite expression and use for the treatment of obesity. Drugs. 2007. doi:10.2165/00003495-200767010-00004 · PMID 17209663
  47. Journal / agency Hurren KM, Berlie HD. Lorcaserin: an investigational serotonin 2C agonist for weight loss. American Journal of Health-System Pharmacy. November 2011. doi:10.2146/ajhp100638 · PMID 22011982
  48. Journal / agency Halford JC, Boyland EJ, Lawton CL, Blundell JE, Harrold JA. Serotonergic anti-obesity agents: past experience and future prospects. Drugs. December 2011. doi:10.2165/11596680-000000000-00000 · PMID 22085383
  49. Journal / agency Halford JC, Harrold JA. Handbook of Experimental Pharmacology. 2012. doi:10.1007/978-3-642-24716-3_16 · PMID 22249823
  50. Journal / agency Przegaliński E, Witek K, Wydra K, Kotlińska JH, Filip M. 5-HT2C Receptor Stimulation in Obesity Treatment: Orthosteric Agonists vs. Allosteric Modulators. Nutrients. March 2023. doi:10.3390/nu15061449 · PMID 36986191 · PMC10058696
  51. Journal / agency Dini G, Di Cara G, Ferrara P, Striano P, Verrotti A. Reintroducing Fenfluramine as a Treatment for Seizures: Current Knowledge, Recommendations and Gaps in Understanding. Neuropsychiatric Disease and Treatment. 2023. doi:10.2147/NDT.S417676 · PMID 37790801 · PMC10543412
  52. Journal / agency Bialer M, Perucca E. Lorcaserin for Dravet Syndrome: A Potential Advance Over Fenfluramine?. CNS Drugs. February 2022. doi:10.1007/s40263-022-00896-3 · PMID 35094259
  53. Journal / agency Dell'isola GB, Verrotti A, Sciaccaluga M, Roberti R, Parnetti L, Russo E, Costa C. Evaluating bexicaserin for the treatment of developmental epileptic encephalopathies. Expert Opinion on Pharmacotherapy. June 2024. doi:10.1080/14656566.2024.2373350 · PMID 38916481
  54. Journal / agency BMB 101. 23 October 2024
  55. Journal / agency Slocum ST, DiBerto JF, Roth BL. Molecular insights into psychedelic drug action. Journal of Neurochemistry. July 2022. doi:10.1111/jnc.15540 · PMID 34797943
  56. Journal / agency Duan W, Cao D, Wang S, Cheng J. Serotonin 2A Receptor (5-HT2AR) Agonists: Psychedelics and Non-Hallucinogenic Analogues as Emerging Antidepressants. Chemical Reviews. January 2024. doi:10.1021/acs.chemrev.3c00375 · PMID 38033123
  57. Journal / agency Nichols DE. Chemistry and Structure-Activity Relationships of Psychedelics. 2018. doi:10.1007/7854_2017_475 · PMID 28401524
  58. Journal / agency Halman A, Kong G, Sarris J, Perkins D. Drug-drug interactions involving classic psychedelics: A systematic review. Journal of Psychopharmacology. January 2024. doi:10.1177/02698811231211219 · PMID 37982394 · PMC10851641
  59. Journal / agency Vargas MV, Dunlap LE, Dong C, Carter SJ, Tombari RJ, Jami SA, Cameron LP, Patel SD, Hennessey JJ, Saeger HN, McCorvy JD, Gray JA, Tian L, Olson DE. Psychedelics promote neuroplasticity through the activation of intracellular 5-HT2A receptors. Science. February 2023. doi:10.1126/science.adf0435 · PMID 36795823 · PMC10108900
  60. Journal / agency Sapienza J. The Key Role of Intracellular 5-HT2A Receptors: A Turning Point in Psychedelic Research?. Psychoactives. 13 October 2023. doi:10.3390/psychoactives2040018
  61. Journal / agency Schmid CL, Bohn LM. 5-HT2A Receptors in the Central Nervous System. 2018. doi:10.1007/978-3-319-70474-6_2
  62. Journal / agency Kozlenkov A, González-Maeso J. The Neuroscience of Hallucinations. 2013. doi:10.1007/978-1-4614-4121-2_14
  63. Journal / agency Schmid CL, Bohn LM. Serotonin, but not N-methyltryptamines, activates the serotonin 2A receptor via a β-arrestin2/Src/Akt signaling complex in vivo. The Journal of Neuroscience. October 2010. doi:10.1523/JNEUROSCI.1665-10.2010 · PMID 20926677 · PMC3001293
  64. Journal / agency Halberstadt AL, Geyer MA. Behavioral Neurobiology of Psychedelic Drugs. 2018. doi:10.1007/7854_2016_466 · PMID 28224459 · PMC5787039
  65. Journal / agency Pévet P. Is 5-methoxytryptamine a pineal hormone?. Psychoneuroendocrinology. 1983. doi:10.1016/0306-4530(83)90041-0 · PMID 6136058
  66. Journal / agency Tan DX, Hardeland R, Back K, Manchester LC, Alatorre-Jimenez MA, Reiter RJ. On the significance of an alternate pathway of melatonin synthesis via 5-methoxytryptamine: comparisons across species. Journal of Pineal Research. August 2016. doi:10.1111/jpi.12336 · PMID 27112772
  67. Journal / agency Przegaliński E, Zebrowska-Lupina I, Wójcik A, Kleinrok Z. 5-Methoxytryptamine-induced head twitches in rats. Polish Journal of Pharmacology and Pharmacy. 1977. PMID 267911
  68. Journal / agency Jiménez JH, Bouso JC. Significance of mammalian N, N-dimethyltryptamine (DMT): A 60-year-old debate. Journal of Psychopharmacology. August 2022. doi:10.1177/02698811221104054 · PMID 35695604
  69. Journal / agency Barker SA. N, N-Dimethyltryptamine (DMT), an Endogenous Hallucinogen: Past, Present, and Future Research to Determine Its Role and Function. Frontiers in Neuroscience. 2018. doi:10.3389/fnins.2018.00536 · PMID 30127713 · PMC6088236
  70. Journal / agency Cameron LP, Olson DE. Dark Classics in Chemical Neuroscience: N, N-Dimethyltryptamine (DMT). ACS Chemical Neuroscience. October 2018. doi:10.1021/acschemneuro.8b00101 · PMID 30036036
  71. Journal / agency Dunlap LE, Andrews AM, Olson DE. Dark Classics in Chemical Neuroscience: 3,4-Methylenedioxymethamphetamine. ACS Chemical Neuroscience. October 2018. doi:10.1021/acschemneuro.8b00155 · PMID 30001118 · PMC6197894
  72. Journal / agency Nichols DE. Entactogens: How the Name for a Novel Class of Psychoactive Agents Originated. Frontiers in Psychiatry. 2022. doi:10.3389/fpsyt.2022.863088 · PMID 35401275 · PMC8990025
  73. Journal / agency Sarparast A, Thomas K, Malcolm B, Stauffer CS. Drug-drug interactions between psychiatric medications and MDMA or psilocybin: a systematic review. Psychopharmacology. June 2022. doi:10.1007/s00213-022-06083-y · PMID 35253070 · PMC9177763
  74. Journal / agency Rothman RB, Baumann MH. Therapeutic potential of monoamine transporter substrates. Current Topics in Medicinal Chemistry. 2006. doi:10.2174/156802606778249766 · PMID 17017961
  75. Journal / agency Scorza C, Silveira R, Nichols DE, Reyes-Parada M. Effects of 5-HT-releasing agents on the extracellullar hippocampal 5-HT of rats. Implications for the development of novel antidepressants with a short onset of action. Neuropharmacology. July 1999. doi:10.1016/S0028-3908(99)00023-4 · PMID 10428424
  76. Journal / agency Marona-Lewicka D, Nichols DE. The Effect of Selective Serotonin Releasing Agents in the Chronic Mild Stress Model of Depression in Rats. Stress. December 1997. doi:10.3109/10253899709014740 · PMID 9787258
  77. Journal / agency Marona-Lewicka D, Nichols DE. Drug discrimination studies of the interoceptive cues produced by selective serotonin uptake inhibitors and selective serotonin releasing agents. Psychopharmacology. July 1998. doi:10.1007/s002130050646 · PMID 9694528
  78. Journal / agency Simmler LD, Liechti ME. New Psychoactive Substances. 2018. doi:10.1007/164_2018_113 · PMID 29633178
  79. Journal / agency Oeri HE. Beyond ecstasy: Alternative entactogens to 3,4-methylenedioxymethamphetamine with potential applications in psychotherapy. Journal of Psychopharmacology. May 2021. doi:10.1177/0269881120920420 · PMID 32909493 · PMC8155739
  80. Journal / agency New AM, Nelson S, Leung JG. Psychiatric Emergencies in the Intensive Care Unit. AACN Advanced Critical Care. 2015-10-01. doi:10.4037/NCI.0000000000000104 · PMID 26484986
  81. Journal / agency Isbister GK, Bowe SJ, Dawson A, Whyte IM. Relative toxicity of selective serotonin reuptake inhibitors (SSRIs) in overdose. Journal of Toxicology. Clinical Toxicology. 2004. doi:10.1081/CLT-120037428 · PMID 15362595
  82. Journal / agency Scotton WJ, Hill LJ, Williams AC, Barnes NM. Serotonin Syndrome: Pathophysiology, Clinical Features, Management, and Potential Future Directions. International Journal of Tryptophan Research. 2019. doi:10.1177/1178646919873925 · PMID 31523132 · PMC6734608
  83. Journal / agency Ordak M, Zmysłowska A, Bielski M, Rybak D, Tomaszewska M, Wyszomierska K, Kmiec A, Garlicka N, Zalewska M, Zalewski M, Nasierowski T, Muszynska E, Bujalska-Zadrozny M. Pharmacotherapy of Patients Taking New Psychoactive Substances: A Systematic Review and Analysis of Case Reports. Frontiers in Psychiatry. 2021. doi:10.3389/fpsyt.2021.669921 · PMID 33967865 · PMC8102790
  84. Journal / agency Jacobs ET, Akers KG, Vohra V, King AM. Cyproheptadine for Serotonin Toxicity: an Updated Systematic Review and Grading of Evidence. Current Emergency and Hospital Medicine Reports. 10 October 2020. doi:10.1007/s40138-020-00222-5
  85. Journal / agency Dunkley EJ, Isbister GK, Sibbritt D, Dawson AH, Whyte IM. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity. QJM. September 2003. doi:10.1093/qjmed/hcg109 · PMID 12925718
  86. Journal / agency Frank C. Recognition and treatment of serotonin syndrome. Canadian Family Physician Medecin de Famille Canadien. July 2008. PMID 18625822 · PMC2464814
  87. Journal / agency Boyer EW, Shannon M. The serotonin syndrome. The New England Journal of Medicine. March 2005. doi:10.1056/NEJMra041867 · PMID 15784664
  88. Other Baskin SI. Principles of cardiac toxicology. 1991
  89. Other Jähnichen S, Horowski R, Pertz H. Pergolide and Cabergoline But not Lisuride Exhibit Agonist Efficacy at Serotonin 5-HT2B Receptors
  90. Journal / agency Adverse Drug Reactions Advisory Committee, Australia. Cardiac valvulopathy with pergolide. Aust Adv Drug React Bull. 2004
  91. Journal / agency Schade R, Andersohn F, Suissa S, Haverkamp W, Garbe E. Dopamine agonists and the risk of cardiac-valve regurgitation. The New England Journal of Medicine. January 2007. doi:10.1056/NEJMoa062222 · PMID 17202453
  92. Journal / agency Zanettini R, Antonini A, Gatto G, Gentile R, Tesei S, Pezzoli G. Valvular heart disease and the use of dopamine agonists for Parkinson's disease. The New England Journal of Medicine. January 2007. doi:10.1056/NEJMoa054830 · PMID 17202454
  93. Journal / agency Pergolide (marketed as Permax) Information. 3 November 2018
  94. Journal / agency MedWatch – 2007 Safety Information Alerts. Permax (pergolide) and generic equivalents. 29 March 2007

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