|Jmol-3D images||Image 1|
|Molar mass||176.215 g/mol|
121–122°C (ligroin) 
416 ±30.0°C (at 760 Torr) 
|Solubility in water||slightly soluble|
|Dipole moment||2.98 D|
|LD50||750 mg/kg (subcutaneous, rat), 4500 mg/kg (intraperitoneal, rat), 60 mg/kg (oral, rat)|
| (what is: / ?)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Serotonin (pron.: //) or 5-hydroxytryptamine (5-HT) is a monoamine neurotransmitter. Biochemically derived from tryptophan, serotonin is primarily found in the gastrointestinal (GI) tract, platelets, and in the central nervous system (CNS) of animals including humans. It is popularly thought to be a contributor to feelings of well-being and happiness.
Approximately 90% of the human body's total serotonin is located in the enterochromaffin cells in the alimentary canal (gut), where it is used to regulate intestinal movements. 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 disgorge serotonin, where it serves as a vasoconstrictor and helps to regulate hemostasis and blood clotting. Serotonin also is a growth factor for some types of cells, which may give it a role in wound healing.
Serotonin is mainly metabolized 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. One type of tumor, called carcinoid, sometimes secretes large amounts of serotonin into the blood, which causes various forms of the carcinoid syndrome of flushing, diarrhea, and heart problems. Because of serotonin's growth-promoting effect on cardiac myocytes, persons with serotonin-secreting carcinoid may suffer a right heart (tricuspid) valve disease syndrome, caused by proliferation of myocytes onto the valve.
In addition to animals, serotonin is found 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. Serotonin is produced by pathogenic amoebae, and its effect on the gut causes diarrhea. Its widespread presence in many seeds and fruits may serve to stimulate the digestive tract into expelling the seeds.
Serotonin is a neurotransmitter and is found in all bilateral animals, where it mediates gut movements and the animals' perceptions of resource availability. In the simplest animals, resources are equivalent with food, but in advanced animals, such as arthropods and vertebrates, resources also can mean social dominance. In response to the perceived abundance or scarcity of resources, an animal's growth, reproduction or mood may be elevated or lowered.
Gauge of food availability (appetite) 
Serotonin functions as a neurotransmitter in the nervous systems of simple, as well as complex, animals. For example, in the roundworm Caenorhabditis elegans, which feeds on bacteria, serotonin is released as a signal in response to positive events, e.g., finding a new source of food or in male animals finding a female with which to mate. 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. The released serotonin activates the muscles used for feeding, while octopamine suppresses them. Serotonin diffuses to serotonin-sensitive neurons, which control the animal's perception of nutrient availability. 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 which block 5-HT2C receptors make the body unable to shut off appetite, and are associated with increased weight gain, especially in people who have a low number of receptors. The expression of 5-HT2C receptors in the hippocampus follows a diurnal rhythm, just as the serotonin release in the ventromedial nucleus, which is characterised by a peak at morning when the motivation to eat is strongest.
Effects of food content 
In humans, serotonin levels are affected by diet. An increase in the ratio of tryptophan to phenylalanine and leucine will increase serotonin levels. Fruits with a good ratio include dates, papayas and bananas. Research also suggests eating a diet rich in carbohydrates and low in protein will increase serotonin by secreting insulin, which helps in amino acid competition. However, increasing insulin for a long period may trigger the onset of insulin resistance, obesity, type 2 diabetes, and lower serotonin levels. Muscles use many of the amino acids except tryptophan, allowing more muscular individuals to produce more serotonin.
In the digestive tract (emetic) 
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 5HT3 receptors in the chemoreceptor trigger zone that stimulate vomiting. The enterochromaffin cells not only react to bad food, but they 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.
How much food an animal gets not only depends on the abundance of food, 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. Thus, serotonin is not only involved in the perception of food availability, but also of social rank. If a lobster is injected with serotonin, it behaves like a dominant animal, while octopamine causes subordinate behavior. A frightened crayfish flips its tail to flee, and the effect of serotonin on this behavior depends 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. In humans, levels of 5-HT1A receptor activation in the brain show negative correlation with aggression, and a mutation in the gene that codes for the 5-HT2A receptor may double the risk of suicide for those with that genotype. Most of the brain serotonin is not 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.
Growth and reproduction 
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. Serotonin is necessary for normal nematode male mating behavior, and the inclination to leave food to search for a mate. 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, which control long-term adaption.
Serotonin is known to regulate aging, learning and memory. The first evidence comes from the study of longevity in C. elegans. During early phase of aging, the level of serotonin increases, which alters locomotory behaviors and associative memory. 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 phase of aging.
Bone metabolism 
In mice and humans, alterations in serotonin levels and signalling have been shown to regulate bone mass. 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 Htr1b receptors, it negatively regulates bone mass, while it does so positively through Htr2b and Htr2c. 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. These studies have opened a new area of research in bone metabolism that can be potentially harnessed to treat bone mass disorders.
In the fruitfly, where insulin both regulates blood sugar and acts as a growth factor, serotonergic neurons regulate the adult body size by affecting insulin secretion. Serotonin has also been identified as the trigger for swarm behavior in locusts. In humans, though insulin regulates blood sugar and IGF regulates growth, serotonin controls the release of both hormones, so serotonin suppresses insulin release from the beta cells in the pancreas, and exposure to SSRIs reduces fetal growth. Human serotonin can also act as a growth factor directly. Liver damage increases cellular expression of 5-HT2A and 5-HT2B receptors. Serotonin present in the blood then stimulates cellular growth to repair liver damage. 5HT2B receptors also activate osteocytes, which build up bone However, serotonin also inhibits osteoblasts, through 5-HT1B receptors.
Cardiovascular growth factor 
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. 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.
Some serotonergic agonist drugs also cause fibrosis anywhere in the body, particularly the syndrome of retroperitoneal fibrosis, as well as cardiac valve fibrosis. In the past, three groups of serotonergic drugs have been epidemiologically linked with these syndromes. They 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. 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 reported in 2003 to be associated with cardiac fibrosis. 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 U.S. market in March, 2007. (Since cabergoline is not approved in the U.S. 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).
Local effects of injection: venoms and pain 
Since serotonin is an indicator of bleeding, a sudden large increase in peripheral levels causes pain. The reason wasps and deathstalker scorpions have serotonin in their venom  may be to increase the pain of their stings on large animals, and also to cause lethal vasoconstriction in smaller prey.
Serotonin in mammals is made by two different tryptophan hydroxylases: TPH1 produces serotonin in the pineal gland and the enterochromaffin cells, while TPH2 produces it in the raphe nuclei and in the myenteric plexus. Genetically altered mice lacking TPH1 develop progressive loss of heart strength early on. They have pale skin and breathing difficulties, are easily tired, and eventually die of heart failure. Genetically altered mice that lack TPH2 are normal when they are born. However, after three days, they appear to be smaller and weaker, and have softer skin than their siblings. In a purebred strain, 50% of the mutants died during the first four weeks, but in a mixed strain, 90% survived. Normally, the mother weans the litter after three weeks, but the mutant animals needed five weeks. After that, they caught up in growth and had normal mortality rates. Subtle changes in the autonomic nervous system are present, but the most obvious difference from normal mice is the increased aggressiveness and impairment in maternal care of young. Despite the blood–brain barrier, the loss of serotonin production in the brain is partially compensated by intestinal serotonin. The behavioural changes become greatly enhanced if one crosses TPH1- with TPH2-lacking mice and gets animals that lack TPH entirely.
In humans, defective signaling of serotonin in the brain may be the root cause of sudden infant death syndrome (SIDS). Scientists from the European Molecular Biology Laboratory in Monterotondo, Italy genetically modified lab mice to produce low levels of the neurotransmitter 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. Researchers now believe low levels of serotonin in the animals' brainstems, which control heartbeat and breathing, may have caused sudden death, they said in the July 4, 2008 issue of Science. If neurons that make serotonin — serotonergic neurons — are abnormal in infants, there is a risk of sudden infant death syndrome (SIDS).
Recent research conducted at Rockefeller University shows, in both patients who suffer from depression and mice that model the disorder, levels of the p11 protein are decreased. This protein is related to serotonin transmission within the brain.
In the brain 
Gross anatomy 
The neurons of the raphe nuclei are the principal source of 5-HT release in the brain. There are 7 or 8 raphe nuclei (some scientists chose to group the raphe linearis nuclei into one nucleus), all of which are located along the midline of the brainstem, and centered around the reticular formation. 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.
Serotonin is released into the 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.
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. With the exception of the 5-HT3 receptor, a ligand-gated ion channel, all other 5-HT receptors are G protein-coupled, seven transmembrane (or heptahelical) receptors that activate an intracellular second messenger cascade.
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 MDMA (ecstasy), amphetamine, cocaine, dextromethorphan (an antitussive), tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs). Interestingly, a 2006 study conducted by the University of Washington suggested a newly discovered monoamine transporter, known as PMAT, may account for "a significant percentage of 5-HT clearance". 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." The study also suggests some SSRIs, such as fluoxetine and sertraline, 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).
Serotonin can also signal through a nonreceptor mechanism called serotonylation, in which serotonin modifies proteins. This process underlies serotonin 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. A similar process underlies the pancreatic release of insulin. 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.
In animals including humans, serotonin is synthesized from the amino acid L-tryptophan by a short metabolic pathway consisting of two enzymes: tryptophan hydroxylase (TPH) and amino acid decarboxylase (DDC). 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.
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. 
Serotonin taken orally does not pass into the serotonergic pathways of the central nervous system, because it does not cross the blood–brain barrier. However, tryptophan and its metabolite 5-hydroxytryptophan (5-HTP), from which serotonin is synthesized, can and do 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.
Drugs targeting the 5-HT system 
Psychedelic drugs 
The psychedelic drugs psilocin/psilocybin, DMT, mescaline, and LSD are agonists, primarily at 5HT2A/2C receptors. The empathogen-entactogen MDMA releases serotonin from synaptic vesicles of neurons.
Drugs which alter serotonin levels are used in 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 reuptake 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. The side effects that have become apparent recently include a decrease in bone mass in elderly and increased risk for osteoporosis. However, it is not yet clear whether it is due to SSRI action on peripheral serotonin production and or action in the gut or in the brain. Certain SSRI medications have been shown to lower serotonin levels below the baseline after chronic use, despite initial increases. This has been connected to the observation that the benefit of SSRIs may decrease in selected patients after a long-term treatment. A switch in medication will usually resolve this issue (up to 70% of the time). The novel antidepressant tianeptine, a selective serotonin reuptake "enhancer", has mood-elevating effects. This provides evidence for the theory that serotonin is most likely used to regulate the extent or intensity of moods, rather than level directly correlating with mood. In fact, 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. Therefore, increasing levels of extracellular serotonin may be associated with increased affect, for good or for worse.
Although phobias and depression might be attenuated by serotonin-altering drugs, this does not mean the individual's situation has been improved, but only the individual's perception of the environment. Sometimes, a lower serotonin level might be beneficial, for example in the ultimatum game, where players with normal serotonin levels are more prone to accept unfair offers than participants whose serotonin levels have been artificially lowered.
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. The intensity of the symptoms of serotonin syndrome vary over a wide spectrum, and the milder forms are seen even at nontoxic levels.
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.
In unicellular organisms 
Serotonin is used by a variety of single-cell organisms for various purposes. SSRIs have been found to be toxic to algae. The gastrointestinal parasite Entamoeba histolytica secretes serotonin, causing a sustained secretory diarrhea in some patients. Patients infected with E. histolytica have been found to have highly elevated serum serotonin levels which returned to normal following resolution of the infection. E. histolytica also responds to the presence of serotonin by becoming more virulent. This means serotonin secretion not only serves to increase the spread of enteamoebas by giving the host diarrhea, but also to coordinate their behaviour according to their population density, a phenomenon known as quorum sensing. Outside a host, the density of entoamoebas is low, hence also the serotonin concentration. 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 serotonin concentration increases.
In plants 
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.
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.
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 above). It is also naturally found in Paramuricea clavata, or the Red Sea Fan.
Serotonin and tryptophan have been found in chocolate with varying cocoa contents. The highest serotonin content (2.93 ug g-1) was found in chocolate with 85% cocoa, and the highest tryptophan content (13.27-13.34 ug g-1) was found in 70-85% cocoa. The intermediate in the synthesis from tryptophan to serotonin, 5-hydroxytryptophan, was not found.
Unlike its precursors, 5-HTP and tryptophan, serotonin does not cross the blood–brain barrier, which means ingesting serotonin in the diet has no effect on brain serotonin levels.
Methyl-tryptamines and hallucinogens 
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 MAO-B enzymes 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. Serotonin is also naturally occurring in toad venom.
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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". 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. 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. Synonyms of serotonin include: 5-hydroxytriptamine, thrombotin, enteramin, substance DS, and 3-(β-Aminoethyl)-5-hydroxyindole.
- Pietra, S.;Farmaco, Edizione Scientifica 1958, Vol. 13, pp. 75–9.
- Calculated using Advanced Chemistry Development (ACD/Labs) Software V11.02 (©1994–2011 ACD/Labs)
- Erspamer, Vittorio (1952). Ricerca Scientifica 22: 694–702.
- Tammisto, Tapani (1968). Annales Medicinae Experimentalis et Biologiea Fenniae 46 (3, Pt. 2): 382–4.
- Young SN (2007). "How to increase serotonin in the human brain without drugs". Rev. Psychiatr. Neurosci. 32 (6): 394–99. PMC 2077351. PMID 18043762.
- King MW. "Serotonin". The Medical Biochemistry Page. Indiana University School of Medicine. Retrieved 2009-12-01.
- Berger M, Gray JA, Roth BL (2009). "The expanded biology of serotonin". Annu. Rev. Med. 60: 355–66. doi:10.1146/annurev.med.60.042307.110802. PMID 19630576.
- Kang K, Park S, Kim YS, Lee S, Back K (2009). "Biosynthesis and biotechnological production of serotonin derivatives". Appl. Microbiol. Biotechnol. 83 (1): 27–34. doi:10.1007/s00253-009-1956-1. PMID 19308403.
- Sawin ER, Ranganathan R, Horvitz HR (2000). "C. elegans locomotory rate is modulated by the environment through a dopaminergic pathway and by experience through a serotonergic pathway". Neuron 26 (3): 619–31. doi:10.1016/S0896-6273(00)81199-X. PMID 10896158.
- Niacaris T, Avery L (2003). "Serotonin regulates repolarization of the C. elegans pharyngeal muscle". J. Exp. Biol. 206 (Pt 2): 223–31. doi:10.1242/jeb.00101. PMID 12477893.
- Stahl SM, Mignon L, Meyer JM (2009). "Which comes first: atypical antipsychotic treatment or cardiometabolic risk?". Acta Psychiatr Scand 119 (3): 171–9. doi:10.1111/j.1600-0447.2008.01334.x. PMID 19178394.
- Buckland PR, Hoogendoorn B, Guy CA, Smith SK, Coleman SL, O'Donovan MC (2005). "Low gene expression conferred by association of an allele of the 5-HT2C receptor gene with antipsychotic-induced weight gain". Am J Psychiatry 162 (3): 613–5. doi:10.1176/appi.ajp.162.3.613. PMID 15741483.
- Holmes MC, French KL, Seckl JR (1997). "Dysregulation of diurnal rhythms of serotonin 5-HT2C and corticosteroid receptor gene expression in the hippocampus with food restriction and glucocorticoids". J. Neurosci. 17 (11): 4056–65. PMID 9151722.
- Leibowitz SF (1990). "The role of serotonin in eating disorders". Drugs. 39 Suppl 3: 33–48. doi:10.2165/00003495-199000393-00005. PMID 2197074.
- Young SN (2007). "How to increase serotonin in the human brain without drugs". J Psychiatry Neurosci 32 (6): 394–9. PMC 2077351. PMID 18043762.
- "Insulin Resistance Syndrome (Metabolic Syndrome) Symptoms, Treatments".
- Grossman, Mary H.; Hart, Cheryle R. (2008). The Feel-Good Diet. New York: McGraw-Hill. p. 64. ISBN 0-07-154849-1.
- Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. p. 187. ISBN 0-443-07145-4.
- de Wit R, Aapro M, Blower PR (2005). "Is there a pharmacological basis for differences in 5-HT3-receptor antagonist efficacy in refractory patients?". Cancer Chemother Pharmacol 56 (3): 231–8. doi:10.1007/s00280-005-1033-0. PMID 15838653.
- Kravitz EA (1988). "Hormonal control of behavior: amines and the biasing of behavioral output in lobsters". Science 241 (4874): 1775–81. Bibcode:1988Sci...241.1775K. doi:10.1126/science.2902685. PMID 2902685.
- Yeh SR, Fricke RA, Edwards DH (1996). "The effect of social experience on serotonergic modulation of the escape circuit of crayfish". Science 271 (5247): 366–9. Bibcode:1996Sci...271..366Y. doi:10.1126/science.271.5247.366. PMID 8553075.
- Caspi N, Modai I, Barak P, Waisbourd A, Zbarsky H, Hirschmann S, Ritsner M. (2001 Mar). "Pindolol augmentation in aggressive schizophrenic patients: a double-blind crossover randomized study". Int Clin Psychopharmacol. 16 (2): 111–5. doi:10.1097/00004850-200103000-00006. PMID 11236069.
- Basky, Greg (2000). "Suicide linked to serotonin gene". CMAJ 162 (9): 1343.
- Lesch KP, Bengel D, Heils A, Sabol SZ, Greenberg BD, Petri S, Benjamin J, Müller CR, Hamer DH, Murphy DL (1996). "Association of anxiety-related traits with a polymorphism in the serotonin transporter gene regulatory region". Science 274 (5292): 1527–31. Bibcode:1996Sci...274.1527L. doi:10.1126/science.274.5292.1527. PMID 8929413.
- Srinivasan S, Sadegh L, Elle IC, Christensen AG, Faergeman NJ, Ashrafi K (2008). "Serotonin regulates C. elegans fat and feeding through independent molecular mechanisms". Cell Metab. 7 (6): 533–44. doi:10.1016/j.cmet.2008.04.012. PMC 2495008. PMID 18522834.
- Loer CM, Kenyon CJ (1993). "Serotonin-deficient mutants and male mating behavior in the nematode Caenorhabditis elegans". J. Neurosci. 13 (12): 5407–17. PMID 8254383.
- Lipton J, Kleemann G, Ghosh R, Lints R, Emmons SW (2004). "Mate searching in Caenorhabditis elegans: a genetic model for sex drive in a simple invertebrate". J. Neurosci. 24 (34): 7427–34. doi:10.1523/JNEUROSCI.1746-04.2004. PMID 15329389.
- Murakami H, Bessinger K, Hellmann J, Murakami S. Aging-dependent and -independent modulation of associative learning behavior by insulin/insulin-like growth factor-1 signal in Caenorhabditis elegans. J Neurosci. 2005 Nov 23;25(47):10894-904. PMID 16306402
- Murakami H, Murakami S (August 2007). "Serotonin receptors antagonistically modulate Caenorhabditis elegans longevity". Aging Cell 6 (4): 483–8. doi:10.1111/j.1474-9726.2007.00303.x. PMID 17559503.
- Murakami H, Bessinger K, Hellmann J, Murakami S (July 2008). "Manipulation of serotonin signal suppresses early phase of behavioral aging in Caenorhabditis elegans". Neurobiol. Aging 29 (7): 1093–100. doi:10.1016/j.neurobiolaging.2007.01.013. PMID 17336425.
- Frost M, Andersen TE, Yadav V, Brixen K, Karsenty G, Kassem M (2010). "Patients with high-bone-mass phenotype owing to Lrp5-T253I mutation have low plasma levels of serotonin". J Bone Miner Res. 25 (3): 673–5. doi:10.1002/jbmr.44. PMID 20200960.
- Rosen CJ (2009). "Breaking into bone biology: serotonin's secrets". Nat Med. 15 (2): 145–6. doi:10.1038/nm0209-145. PMID 19197289.
- Mödder UI, Achenbach SJ, Amin S, Riggs BL, Melton LJ 3rd, Khosla S (2010). "Relation of serum serotonin levels to bone density and structural parameters in women". J Bone Miner Res. 25 (2): 415–22. doi:10.1359/jbmr.090721. PMC 3153390. PMID 19594297.
- Frost M, Andersen T, Gossiel F, Hansen S, Bollerslev J, Van Hul W, Eastell R, Kassem M, Brixen K. (2011). "Levels of serotonin, sclerostin, bone turnover markers as well as bone density and microarchitecture in patients with high bone mass phenotype due to a mutation in Lrp5". J Bone Miner Res. 26 (8): 1721–8. doi:10.1002/jbmr.376. PMID 21351148.
- Kode A, Mosialou I, Silva BC, Rached MT, Zhou B, Wang J, Townes TM, Hen R, Depinho RA, Guo XE, Kousteni S. (2012). "FOXO1 orchestrates the bone-suppressing function of gut-derived serotonin". J Clin Invest. 122 (10): 3490–503. doi:10.1172/JCI64906. PMC 3461930. PMID 22945629.
- Yadav VK, Balaji S, Suresh PS, Liu XS, Lu X, Li Z, Guo XE, Mann JJ, Balapure AK, Gershon MD, Medhamurthy R, Vidal M, Karsenty G, Ducy P. (2010). "Pharmacological inhibition of gut-derived serotonin synthesis is a potential bone anabolic treatment for osteoporosis". Nat Med. 16 (3): 308–12. doi:10.1038/nm.2098. PMC 2836724. PMID 20139991.
- Kaplan DD, Zimmermann G, Suyama K, Meyer T, Scott MP (2008). "A nucleostemin family GTPase, NS3, acts in serotonergic neurons to regulate insulin signaling and control body size". Genes Dev. 22 (14): 1877–93. doi:10.1101/gad.1670508. PMC 2492735. PMID 18628395.
- Ruaud AF, Thummel CS (2008). "Serotonin and insulin signaling team up to control growth in Drosophila". Genes Dev. 22 (14): 1851–5. doi:10.1101/gad.1700708. PMC 2735276. PMID 18628391.
- Anstey ML, Rogers SM, Ott SR, Burrows M, Simpson SJ (2009). "Serotonin mediates behavioral gregarization underlying swarm formation in desert locusts". Science 323 (5914): 627–30. Bibcode:2009Sci...323..627A. doi:10.1126/science.1165939. PMID 19179529. Lay summary – BBC News.
- Paulmann N, Grohmann M, Voigt JP, Bert B, Vowinckel J, Bader M, Skelin M, Jevsek M, Fink H, Rupnik M, Walther DJ (2009). "Intracellular serotonin modulates insulin secretion from pancreatic beta-cells by protein serotonylation". In O'Rahilly, Steve. PLoS Biol. 7 (10): e1000229. doi:10.1371/journal.pbio.1000229. PMC 2760755. PMID 19859528.
- Davidson S, Prokonov D, Taler M, Maayan R, Harell D, Gil-Ad I, Weizman A (2009). "Effect of exposure to selective serotonin reuptake inhibitors in utero on fetal growth: potential role for the IGF-I and HPA axes". Pediatr. Res. 65 (2): 236–41. doi:10.1203/PDR.0b013e318193594a. PMID 19262294.
- Lesurtel M, Graf R, Aleil B, Walther DJ, Tian Y, Jochum W, Gachet C, Bader M, Clavien PA (2006). "Platelet-derived serotonin mediates liver regeneration". Science 312 (5770): 104–7. Bibcode:2006Sci...312..104L. doi:10.1126/science.1123842. PMID 16601191.
- Matondo RB, Punt C, Homberg J, Toussaint MJ, Kisjes R, Korporaal SJ, Akkerman JW, Cuppen E, de Bruin A (2009). "Deletion of the serotonin transporter in rats disturbs serotonin homeostasis without impairing liver regeneration". Am. J. Physiol. Gastrointest. Liver Physiol. 296 (4): G963–8. doi:10.1152/ajpgi.90709.2008. PMID 19246633.
- Collet C, Schiltz C, Geoffroy V, Maroteaux L, Launay JM, de Vernejoul MC (2008). "The serotonin 5-HT2B receptor controls bone mass via osteoblast recruitment and proliferation". FASEB J. 22 (2): 418–27. doi:10.1096/fj.07-9209com. PMID 17846081.
- Yadav VK, Ryu JH, Suda N, Tanaka KF, Gingrich JA, Schütz G, Glorieux FH, Chiang CY, Zajac JD, Insogna KL, Mann JJ, Hen R, Ducy P, Karsenty G (2008). "Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum". Cell 135 (5): 825–37. doi:10.1016/j.cell.2008.09.059. PMC 2614332. PMID 19041748. Lay summary – Science Daily.
- McDuffie JE, Motley ED, Limbird LE, Maleque MA (2000). "5-hydroxytryptamine stimulates phosphorylation of p44/p42 mitogen-activated protein kinase activation in bovine aortic endothelial cell cultures". J. Cardiovasc. Pharmacol. 35 (3): 398–402. doi:10.1097/00005344-200003000-00008. PMID 10710124.
- Marieb, Elaine Nicpon (2009). Essentials of human anatomy & physiology (Eighth ed.). San Francisco: Pearson/Benjamin Cummings. p. 336. ISBN 0-321-51342-8.
- Baskin SI (1991). Principles of cardiac toxicology. Boca Raton: CRC Press. ISBN 0-8493-8809-0. Retrieved 2010-02-03.
- Jähnichen S, Horowski R, Pertz H. "Pergolide and Cabergoline But not Lisuride Exhibit Agonist Efficacy at Serotonin 5-HT2B Receptors". Retrieved 2010-02-03.
- ADRAC (2004). "Cardiac valvulopathy with pergolide". Aust Adv Drug React Bull 23 (4). Free full text from the Australian Therapeutic Goods Administration
- Schade R, Andersohn F, Suissa S, Haverkamp W, Garbe E (2007). "Dopamine agonists and the risk of cardiac-valve regurgitation". N. Engl. J. Med. 356 (1): 29–38. doi:10.1056/NEJMoa062222. PMID 17202453.
- Zanettini R, Antonini A, Gatto G, Gentile R, Tesei S, Pezzoli G (2007). "Valvular heart disease and the use of dopamine agonists for Parkinson's disease". N. Engl. J. Med. 356 (1): 39–46. doi:10.1056/NEJMoa054830. PMID 17202454.
- "Food and Drug Administration Public Health Advisory". 2007-03-29. Retrieved 2010-02-07.
- "MedWatch – 2007 Safety Information Alerts. Permax (pergolide) and generic equivalents". U.S. Food and Drug Administration. March 29, 2007. Retrieved 2007-03-30.
- Jaques R, Schachter M (1954). "The presence of histamine, 5-hydroxytryptamine and a potent, slow contracting substance in wasp venom". Br J Pharmacol Chemother 9 (1): 53–8. doi:10.1111/j.1476-5381.1954.tb00816.x. PMC 1509391. PMID 13149776.
- Adam KR, Weiss C (1959). "Distribution of 5-hydroxytryptamine in scorpion venoms". Nature 183 (4672): 1398–9. Bibcode:1959Natur.183.1398A. doi:10.1038/1831398a0. PMID 13657136.
- Ben Arous J, Laffont S, Chatenay D (2009). "Molecular and sensory basis of a food related two-state behavior in C. elegans". In Brezina, Vladimir. PLoS ONE 4 (10): e7584. Bibcode:2009PLoSO...4.7584B. doi:10.1371/journal.pone.0007584. PMC 2762077. PMID 19851507.
- Sze JY, Victor M, Loer C, Shi Y, Ruvkun G (2000). "Food and metabolic signaling defects in a Caenorhabditis elegans serotonin-synthesis mutant". Nature 403 (6769): 560–4. Bibcode:2000Natur.403..560S. doi:10.1038/35000609. PMID 10676966.
- Côté F, Thévenot E, Fligny C et al. (2003). "Disruption of the nonneuronal tph1 gene demonstrates the importance of peripheral serotonin in cardiac function". Proc. Natl. Acad. Sci. U.S.A. 100 (23): 13525–30. Bibcode:2003PNAS..10013525C. doi:10.1073/pnas.2233056100. PMC 263847. PMID 14597720.
- Alenina N, Kikic D, Todiras M, Mosienko V, Qadri F, Plehm R, Boyé P, Vilianovitch L, Sohr R, Tenner K, Hörtnagl H, Bader M (2009). "Growth retardation and altered autonomic control in mice lacking brain serotonin". Proc. Natl. Acad. Sci. U.S.A. 106 (25): 10332–7. Bibcode:2009PNAS..10610332A. doi:10.1073/pnas.0810793106. PMC 2700938. PMID 19520831.
- Savelieva KV, Zhao S, Pogorelov VM et al. (2008). "Genetic disruption of both tryptophan hydroxylase genes dramatically reduces serotonin and affects behavior in models sensitive to antidepressants". In Bartolomucci, Alessandro. PLoS ONE 3 (10): e3301. Bibcode:2008PLoSO...3.3301S. doi:10.1371/journal.pone.0003301. PMC 2565062. PMID 18923670.
- Audero, Enrica; Coppi, Elisabetta; Mlinar, Boris; Rossetti, Tiziana; Caprioli, Antonio; Al Banchaabouchi, Mumna; Corradetti, Renato; Gross, Cornelius (2008). "Sporadic Autonomic Dysregulation and Death Associated with Excessive Serotonin Autoinhibition". Science 321 (5885): 130–133. Bibcode:2008Sci...321..130A. doi:10.1126/science.1157871. PMID 18599790.
- Paterson DS, Trachtenberg FL, Thompson EG, Belliveau RA, Beggs AH, Darnall R, Chadwick AE, Krous HF, Kinney HC (2006). "Multiple serotonergic brainstem abnormalities in sudden infant death syndrome". JAMA 296 (17): 2124–32. doi:10.1001/jama.296.17.2124. PMID 17077377.
- Svenningsson P, Chergui K, Rachleff I, Flajolet M, Zhang X, El Yacoubi M, Vaugeois JM, Nomikos GG, Greengard P (2006). "Alterations in 5-HT1B receptor function by p11 in depression-like states". Science 311 (5757): 77–80. Bibcode:2006Sci...311...77S. doi:10.1126/science.1117571. PMID 16400147.
- Frazer, A.; and Hensler, J. G. (1999). "Understanding the neuroanatomical organization of serotonergic cells in the brain provides insight into the functions of this neurotransmitter". In Siegel, G. J.. Basic Neurochemistry. Agranoff, Bernard W.; Fisher, Stephen K.; Albers, R. Wayne; Uhler, Michael D. (Sixth ed.). Lippincott Williams and Wilkins. ISBN 0-397-51820-X. "In 1964, Dahlstrom and Fuxe (discussed in ), using the Falck-Hillarp technique of histofluorescence, observed that the majority of serotonergic soma are found in cell body groups, which previously had been designated as the raphe nuclei."
- The Raphe nuclei group of neurons are located along the brain stem from the labels 'Mid Brain' to 'Oblongata', centered on the pons. (See relevant image.)
- Hannon J, Hoyer D (2008). "Molecular biology of 5-HT receptors". Behav. Brain Res. 195 (1): 198–213. doi:10.1016/j.bbr.2008.03.020. PMID 18571247.
- Walther DJ, Peter JU, Winter S, Höltje M, Paulmann N, Grohmann M, Vowinckel J, Alamo-Bethencourt V, Wilhelm CS, Ahnert-Hilger G, Bader M (2003). "Serotonylation of small GTPases is a signal transduction pathway that triggers platelet alpha-granule release". Cell 115 (7): 851–62. doi:10.1016/S0092-8674(03)01014-6. PMID 14697203.
- Watts SW, Priestley JR, Thompson JM (2009). "Serotonylation of vascular proteins important to contraction". In Kreindler, James L. PLoS ONE 4 (5): e5682. Bibcode:2009PLoSO...4.5682W. doi:10.1371/journal.pone.0005682. PMC 2682564. PMID 19479059.
- Alarcon, J. Biotransformation of indole derivatives by mycelial cultures. Zeitschrift für Naturforschung.C, A journal of biosciences 2008, 63, 82.
- Titeler M, Lyon RA, Glennon RA (1988). "Radioligand binding evidence implicates the brain 5-HT2 receptor as a site of action for LSD and phenylisopropylamine hallucinogens". Psychopharmacology (Berl.) 94 (2): 213–6. doi:10.1007/BF00176847. PMID 3127847.
- Nichols DE (2000). "Role of serotonergic neurons and 5-HT receptors in the action of hallucinogens". In Baumgarten HG, Gothert M. Serotoninergic Neurons and 5-HT Receptors in the CNS. Santa Clara, CA: Springer-Verlag TELOS. ISBN 3-540-66715-6.
- Johnson MP, Hoffman AJ, Nichols DE (1986). "Effects of the enantiomers of MDA, MDMA and related analogues on [3H]serotonin and [3H]dopamine release from superfused rat brain slices". Eur. J. Pharmacol. 132 (2–3): 269–76. doi:10.1016/0014-2999(86)90615-1. PMID 2880735.
- Benmansour S, Cecchi M, Morilak DA, Gerhardt GA, Javors MA, Gould GG, Frazer A (1999). "Effects of chronic antidepressant treatments on serotonin transporter function, density, and mRNA level". J. Neurosci. 19 (23): 10494–501. PMID 10575045.
- Beitchman J, Baldassarra L, Mik H, De Luca V, King N, Bender D, Ehtesham S, Kennedy J (2011). "Serotonin Transporter Polymorphisms and Persistent, Pervasive Childhood Aggression". The American Journal of Psychiatry 163 (6): 1103–5. doi:10.1176/appi.ajp.163.6.1103. PMID 16741214.
- Pezawas, L.; Meyer-Lindenberg, A.; Drabant, E. M.; Verchinski, B. A.; Munoz, K. E.; Kolachana, B. S.; Egan, M. F.; Mattay, V. S. et al. (2005). "5-HTTLPR polymorphism impacts human cingulate-amygdala interactions: A genetic susceptibility mechanism for depression". Nature Neuroscience 8 (6): 828–834. doi:10.1038/nn1463. PMID 15880108.
- Schinka, J. A.; Busch, R. M.; Robichaux-Keene, N. (2004). "A meta-analysis of the association between the serotonin transporter gene polymorphism (5-HTTLPR) and trait anxiety". Molecular Psychiatry 9 (2): 197–202. doi:10.1038/sj.mp.4001405. PMID 14966478.
- Crockett MJ, Clark L, Tabibnia G, Lieberman MD, Robbins TW (2008). "Serotonin modulates behavioral reactions to unfairness". Science 320 (5884): 1739. Bibcode:2008Sci...320.1739C. doi:10.1126/science.1155577. PMC 2504725. PMID 18535210. Lay summary.
- Isbister, G. K.; Bowe, S. J.; Dawson, A.; Whyte, I. M. (2004). "Relative toxicity of selective serotonin reuptake inhibitors (SSRIs) in overdose". J. Toxicol. Clin. Toxicol. 42 (3): 277–85. doi:10.1081/CLT-120037428. PMID 15362595.
- Dunkley EJ, Isbister GK, Sibbritt D, Dawson AH, Whyte IM (2003). "The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity". QJM 96 (9): 635–42. doi:10.1093/qjmed/hcg109. PMID 12925718.
- Johnson DJ, Sanderson H, Brain RA, Wilson CJ, Solomon KR (2007). "Toxicity and hazard of selective serotonin reuptake inhibitor antidepressants fluoxetine, fluvoxamine, and sertraline to algae". Ecotoxicol. Environ. Saf. 67 (1): 128–39. doi:10.1016/j.ecoenv.2006.03.016. PMID 16753215.
- McGowan K, Kane A, Asarkof N, Wicks J, Guerina V, Kellum J, Baron S, Gintzler AR, Donowitz M (1983). "Entamoeba histolytica causes intestinal secretion: role of serotonin". Science 221 (4612): 762–4. Bibcode:1983Sci...221..762M. doi:10.1126/science.6308760. PMID 6308760.
- McGowan K, Guerina V, Wicks J, Donowitz M (1985). "Secretory hormones of Entamoeba histolytica". Ciba Found. Symp. 112: 139–54. PMID 2861068.
- Banu N, Zaidi KR, Mehdi G, Mansoor T (2005). "Neurohumoral alterations and their role in amoebiasis" (PDF). Indian J. Clin Biochem 20 (2): 142–5. doi:10.1007/BF02867414. PMC 3453840. PMID 23105547.
- Acharya DP, Sen MR, Sen PC (1989). "Effect of exogenous 5-hydroxytryptamine on pathogenicity of Entamoeba histolytica in experimental animals". Indian J. Exp. Biol. 27 (8): 718–20. PMID 2561282.
- Schröder P, Abele C, Gohr P, Stuhlfauth-Roisch U, Grosse W. (1999). "Latest on enzymology of serotonin biosynthesis in walnut seeds". Adv Exp Med Biol. Advances in Experimental Medicine and Biology 467: 637–644. doi:10.1007/978-1-4615-4709-9_81. ISBN 978-0-306-46204-7. PMID 10721112.
- Feldman, J. M.; Lee, E. M. (1985). "Serotonin content of foods: effect on urinary excretion of 5-hydroxyindoleacetic acid". Am. J. Clin. Nutr. 42 (4): 639–43. PMID 2413754.
- Penez, N.; Culioli, G.; Briand, J.; Blache, Y.; Perez, T.; Thomas, O. P. Antifouling Properties of Simple Indole and Purine Alkaloids from the Mediterranean Gorgonian Paramuricea clavata. J. Nat. Prod. 2011, 74, 2304-2308.
- Guillen-Casla, V.; Rosales-Conrado, N.; Leon-Gonzalez, M. E.; Perez-Arribas, L. V.; Polo-Diez, L. M. Determination ofserotonin and its precursors in chocolate samples by capillary liquid chromatography with mass spectrometry detection. J. Chromatogr. A. 2012, 1232, 158-165.
- Tyler Jr, VE (1958). "Occurrence of serotonin in a hallucinogenic mushroom". Science 128 (3326): 718. Bibcode:1958Sci...128..718T. doi:10.1126/science.128.3326.718. PMID 13580242.
- Zhang, P.; Cui, Z.; Liu, Y.; Wang, D.; Liu, N.; Yoshikawa, M. Quality Evaluation of Drug Toad Venom fromDifferent Origins through a Simultaneous Determination of Bufogeninsand Indole Alkaloids by HPLC. Chem. Pharm. Bull. 2005, 53, 1582-1586.
- Negri L (2006). "[Vittorio Erspamer (1909–1999)]". Med Secoli (in Italian) 18 (1): 97–113. PMID 17526278.
- Rapport MM, Green AA, Page IH (1948). "Serum vasoconstrictor, serotonin; isolation and characterization". J. Biol. Chem. 176 (3): 1243–51. PMID 18100415.
- Feldberg W, Toh CC (1953). "Distribution of 5-hydroxytryptamine (serotonin, enteramine) in the wall of the digestive tract". J. Physiol. (Lond.) 119 (2–3): 352–62. PMC 1392800. PMID 13035756.
- SciFinder – Serotonin Substance Detail. Accessed (4-11-2012).
- 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.
- Tryptophan hydroxylase-2 gene variation influences personality traits and disorders related to emotional dysregulation at the National Center for Biotechnology Information.