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Tryptamine

From Wikipedia, the free encyclopedia
This article is about the specific substance. For the class of substances, see substituted tryptamine.
Tryptamine
Names
Preferred IUPAC name
2-(1H-Indol-3-yl)ethan-1-amine
Identifiers
3D model (JSmol)
125513
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard 100.000.464 Edit this at Wikidata
KEGG
UNII
  • InChI=1S/C10H12N2/c11-6-5-8-7-12-10-4-2-1-3-9(8)10/h1-4,7,12H,5-6,11H2 checkY
    Key: APJYDQYYACXCRM-UHFFFAOYSA-N ☒N
  • InChI=1/C10H12N2/c11-6-5-8-7-12-10-4-2-1-3-9(8)10/h1-4,7,12H,5-6,11H2
    Key: APJYDQYYACXCRM-UHFFFAOYAU
  • c1ccc2c(c1)c(c[nH]2)CCN
Properties[1]
C10H12N2
Molar mass 160.220 g·mol−1
Appearance white to orange needles
Melting point 118˚C
Boiling point 137 °C (279 °F; 410 K) (0.15 mmHg)
negligible solubility in water
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

Tryptamine is an indolamine metabolite of the essential amino acid, tryptophan.[2][3] The chemical structure is defined by an indole—a fused benzene and pyrrole ring, and a 2-aminoethyl group at the second carbon (third aromatic atom, with the first one being the heterocyclic nitrogen).[2] The structure of tryptamine is a shared feature of certain aminergic neuromodulators including melatonin, serotonin, bufotenin and psychedelic derivatives such as dimethyltryptamine (DMT), psilocybin, psilocin and others.[4][5][6]

Tryptamine has been shown to activate serotonin receptors[7][8] and trace amine-associated receptors expressed in the mammalian brain, and regulates the activity of dopaminergic, serotonergic and glutamatergic systems.[9][10] In the human gut, symbiotic bacteria convert dietary tryptophan to tryptamine, which activates 5-HT4 receptors and regulates gastrointestinal motility.[3][11][12]

Multiple tryptamine-derived drugs have been developed to treat migraines, while trace amine-associated receptors are being explored as a potential treatment target for neuropsychiatric disorders.[13][14][15]

All tryptamine derivatives possess a modified 2-aminoethyl group and/or the addition of a substituent on the indole.

Natural occurrences

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For a list of plants, fungi and animals containing tryptamines, see List of psychoactive plants and List of naturally occurring tryptamines.

Mammalian brain

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Endogenous levels of tryptamine in the mammalian brain are less than 100 ng per gram of tissue.[16][17] However, elevated levels of trace amines have been observed in patients with certain neuropsychiatric disorders taking medications, such as bipolar depression and schizophrenia.[18]

Mammalian gut microbiome

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Tryptamine is relatively abundant in the gut and feces of humans and rodents.[19][20] Commensal bacteria, including Ruminococcus gnavus and Clostridium sporogenes in the gastrointestinal tract, possess the enzyme tryptophan decarboxylase, which aids in the conversion of dietary tryptophan to tryptamine.[19] Tryptamine is a ligand for gut epithelial serotonin type 4 (5-HT4) receptors and regulates gastrointestinal electrolyte balance through colonic secretions.[20]

Metabolism

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Biosynthesis

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To yield tryptamine in vivo, tryptophan decarboxylase removes the carboxylic acid group on the α-carbon of tryptophan.[21] Synthetic modifications to tryptamine can produce serotonin and melatonin; however, these pathways do not occur naturally as the main pathway for endogenous neurotransmitter synthesis.[22]

Conversion of tryptophan to tryptamine, followed by its degradation to indole-3-acetic acid

Catabolism

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Monoamine oxidases A and B are the primary enzymes involved in tryptamine metabolism to produce indole-3-acetaldehyde, however it is unclear which isoform is specific to tryptamine degradation.[23]

Mechanisms of action and biological effects

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Neuromodulation

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Tryptamine is known to act as a serotonin receptor agonist, although its potency is limited by rapid inactivation by monoamine oxidases.[7][8][24][25] It has specifically been found to act as a full agonist of the serotonin 5-HT2A receptor (EC50Tooltip half-maximal effective concentration = 7.36 ± 0.56 nM; Emax = 104 ± 4%).[7] Tryptamine was of much lower potency in stimulating the 5-HT2A receptor β-arrestin pathway (EC50 = 3,485 ± 234 nM; Emax = 108 ± 16%).[7] In contrast to the 5-HT2A receptor, tryptamine was found to be inactive at the serotonin 5-HT1A receptor.[7] Alexander Shulgin tested tryptamine at high doses intravenously and found that it produced weak serotonergic psychedelic-like effects as well as peripheral nervous system changes.[7][26]

It can also weakly activate the trace amine-associated receptor, TAAR1 (hTAAR1 in humans).[27][28][29] Limited studies have considered tryptamine to be a trace neuromodulator capable of regulating the activity of neuronal cell responses without binding to the associated postsynaptic receptors.[29][30]

Tryptamine has been found to act as a monoamine releasing agent.[7][31] It is a releaser of serotonin, dopamine, and norepinephrine, in that order of potency (EC50 = 32.6 ± 2.6 nM, 164 ± 16 nM, and 716 ± 46 nM, respectively).[7][31] It is also a monoaminergic activity enhancer of these neurotransmitters.[32][33]

hTAAR1

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Tryptamine promotes intestinal motility by activating serotonin receptors in the gut to increase colonic secretions.

hTAAR1 is a stimulatory G-protein coupled receptor (GPCR) that is weakly expressed in the intracellular compartment of both pre- and postsynaptic neurons.[34] Tryptamine and other hTAAR1 agonists can increase neuronal firing by inhibiting neurotransmitter recycling through cAMP-dependent phosphorylation of the monoamine reuptake transporter.[35][30] This mechanism increases the amount of neurotransmitter in the synaptic cleft, subsequently increasing postsynaptic receptor binding and neuronal activation.[30] Conversely, when hTAAR1 are colocalized with G protein-coupled inwardly-rectifying potassium channels (GIRKs), receptor activation reduces neuronal firing by facilitating membrane hyperpolarization through the efflux of potassium ions.[30] The balance between the inhibitory and excitatory activity of hTAAR1 activation highlights the role of tryptamine in the regulation of neural activity.[36]

Activation of hTAAR1 is under investigation as a novel treatment for depression, addiction, and schizophrenia.[37] hTAAR1 is primarily expressed in brain structures associated with dopamine systems, such as the ventral tegmental area (VTA) and serotonin systems in the dorsal raphe nuclei (DRN).[37] Additionally, the hTAAR1 gene is localized at 6q23.2 on the human chromosome, which is a susceptibility locus for mood disorders and schizophrenia.[38] Activation of TAAR1 suggests a potential novel treatment for neuropsychiatric disorders, as TAAR1 agonists produce anti-depressive activity, increased cognition, reduced stress and anti-addiction effects.[36][38]

TAAR1 affinities and activational potencies of tryptamines[39]
Tryptamine Human TAAR1 Mouse TAAR1 Rat TAAR1
EC50 Ki EC50 Ki EC50 Ki
Tryptamine 21 N/A 2.7 1.4 0.41 0.13
Serotonin >50 N/A >50 N/A 5.2 N/A
Psilocin >30 N/A 2.7 17 0.92 1.4
Dimethyltryptamine >10 N/A 1.2 3.3 1.5 22
Notes: (1) EC50 and Ki values are in micromolar (μM). (2) EC50 reflects the concentration required to elicit 50% of the maximum TAAR1 response. (3) The smaller the Ki value, the stronger the compound binds to the receptor.

Monoaminergic activity enhancer

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Tryptamine is a monoaminergic activity enhancer (MAE) of serotonin, norepinephrine, and dopamine in addition to its serotonin receptor agonism.[32][33] That is, it enhances the action potential-mediated release of these monoamine neurotransmitters.[32][33] The MAE actions of tryptamine and other MAEs may be mediated by TAAR1 agonism.[40][41] Synthetic and more potent MAEs like benzofuranylpropylaminopentane (BPAP) and indolylpropylaminopentane (IPAP) have been derived from tryptamine.[32][33][42][43][44]

Gastrointestinal motility

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Tryptamine produced by mutualistic bacteria in the human gut activates serotonin GPCRs ubiquitously expressed along the colonic epithelium.[45] Upon tryptamine binding, the activated 5-HT4 receptor undergoes a conformational change which allows its Gs alpha subunit to exchange GDP for GTP, and its liberation from the 5-HT4 receptor and βγ subunit.[45] GTP-bound Gs activates adenylyl cyclase, which catalyzes the conversion of ATP into cyclic adenosine monophosphate (cAMP).[45] cAMP opens chloride and potassium ion channels to drive colonic electrolyte secretion and promote intestinal motility.[46][47]

See also

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References

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  1. ^ Lide, D. R., ed. (2005). CRC Handbook of Chemistry and Physics (85th ed.). CRC Press. p. 3-564. ISBN 978-0-8493-0484-2.
  2. ^ a b "Tryptamine". pubchem.ncbi.nlm.nih.gov. Retrieved 2020-12-01.
  3. ^ a b Jenkins, Trisha A.; Nguyen, Jason C. D.; Polglaze, Kate E.; Bertrand, Paul P. (2016-01-20). "Influence of Tryptophan and Serotonin on Mood and Cognition with a Possible Role of the Gut-Brain Axis". Nutrients. 8 (1): 56. doi:10.3390/nu8010056. ISSN 2072-6643. PMC 4728667. PMID 26805875.
  4. ^ Tylš, Filip; Páleníček, Tomáš; Horáček, Jiří (2014-03-01). "Psilocybin – Summary of knowledge and new perspectives". European Neuropsychopharmacology. 24 (3): 342–356. doi:10.1016/j.euroneuro.2013.12.006. ISSN 0924-977X. PMID 24444771. S2CID 10758314.
  5. ^ Tittarelli, Roberta; Mannocchi, Giulio; Pantano, Flaminia; Romolo, Francesco Saverio (2015). "Recreational Use, Analysis and Toxicity of Tryptamines". Current Neuropharmacology. 13 (1): 26–46. doi:10.2174/1570159X13666141210222409. ISSN 1570-159X. PMC 4462041. PMID 26074742.
  6. ^ "The Ayahuasca Phenomenon". MAPS. 21 November 2014. Retrieved 2020-10-03.
  7. ^ a b c d e f g h Blough BE, Landavazo A, Decker AM, Partilla JS, Baumann MH, Rothman RB (October 2014). "Interaction of psychoactive tryptamines with biogenic amine transporters and serotonin receptor subtypes". Psychopharmacology (Berl). 231 (21): 4135–4144. doi:10.1007/s00213-014-3557-7. PMC 4194234. PMID 24800892.
  8. ^ a b Mousseau DD (March 1993). "Tryptamine: a metabolite of tryptophan implicated in various neuropsychiatric disorders". Metab Brain Dis. 8 (1): 1–44. doi:10.1007/BF01000528. PMID 8098507.
  9. ^ Khan, Muhammad Zahid; Nawaz, Waqas (2016-10-01). "The emerging roles of human trace amines and human trace amine-associated receptors (hTAARs) in central nervous system". Biomedicine & Pharmacotherapy. 83: 439–449. doi:10.1016/j.biopha.2016.07.002. ISSN 0753-3322. PMID 27424325.
  10. ^ Berry, Mark D.; Gainetdinov, Raul R.; Hoener, Marius C.; Shahid, Mohammed (2017-12-01). "Pharmacology of human trace amine-associated receptors: Therapeutic opportunities and challenges". Pharmacology & Therapeutics. 180: 161–180. doi:10.1016/j.pharmthera.2017.07.002. ISSN 0163-7258. PMID 28723415. S2CID 207366162.
  11. ^ Bhattarai, Yogesh; Williams, Brianna B.; Battaglioli, Eric J.; Whitaker, Weston R.; Till, Lisa; Grover, Madhusudan; Linden, David R.; Akiba, Yasutada; Kandimalla, Karunya K.; Zachos, Nicholas C.; Kaunitz, Jonathan D. (2018-06-13). "Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion". Cell Host & Microbe. 23 (6): 775–785.e5. doi:10.1016/j.chom.2018.05.004. ISSN 1931-3128. PMC 6055526. PMID 29902441.
  12. ^ Field, Michael (2003). "Intestinal ion transport and the pathophysiology of diarrhea". Journal of Clinical Investigation. 111 (7): 931–943. doi:10.1172/JCI200318326. ISSN 0021-9738. PMC 152597. PMID 12671039.
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  17. ^ Berry, Mark D.; Gainetdinov, Raul R.; Hoener, Marius C.; Shahid, Mohammed (2017-12-01). "Pharmacology of human trace amine-associated receptors: Therapeutic opportunities and challenges". Pharmacology & Therapeutics. 180: 161–180. doi:10.1016/j.pharmthera.2017.07.002. ISSN 0163-7258. PMID 28723415. S2CID 207366162.
  18. ^ Miller, Gregory M. (2011). "The Emerging Role of Trace Amine Associated Receptor 1 in the Functional Regulation of Monoamine Transporters and Dopaminergic Activity". Journal of Neurochemistry. 116 (2): 164–176. doi:10.1111/j.1471-4159.2010.07109.x. ISSN 0022-3042. PMC 3005101. PMID 21073468.
  19. ^ a b Jenkins, Trisha A.; Nguyen, Jason C. D.; Polglaze, Kate E.; Bertrand, Paul P. (2016-01-20). "Influence of Tryptophan and Serotonin on Mood and Cognition with a Possible Role of the Gut-Brain Axis". Nutrients. 8 (1): 56. doi:10.3390/nu8010056. ISSN 2072-6643. PMC 4728667. PMID 26805875.
  20. ^ a b Bhattarai, Yogesh; Williams, Brianna B.; Battaglioli, Eric J.; Whitaker, Weston R.; Till, Lisa; Grover, Madhusudan; Linden, David R.; Akiba, Yasutada; Kandimalla, Karunya K.; Zachos, Nicholas C.; Kaunitz, Jonathan D. (2018-06-13). "Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion". Cell Host & Microbe. 23 (6): 775–785.e5. doi:10.1016/j.chom.2018.05.004. ISSN 1931-3128. PMC 6055526. PMID 29902441.
  21. ^ Tittarelli, Roberta; Mannocchi, Giulio; Pantano, Flaminia; Romolo, Francesco Saverio (2015). "Recreational Use, Analysis and Toxicity of Tryptamines". Current Neuropharmacology. 13 (1): 26–46. doi:10.2174/1570159X13666141210222409. ISSN 1570-159X. PMC 4462041. PMID 26074742.
  22. ^ "Serotonin Synthesis and Metabolism". Sigma Aldrich. 2020.
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  25. ^ Bradley PB, Humphrey PP, Williams RH (April 1985). "Tryptamine-induced vasoconstrictor responses in rat caudal arteries are mediated predominantly via 5-hydroxytryptamine receptors". Br J Pharmacol. 84 (4): 919–925. doi:10.1111/j.1476-5381.1985.tb17386.x. PMC 1987057. PMID 3159458.
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  45. ^ a b c Bhattarai, Yogesh; Williams, Brianna B.; Battaglioli, Eric J.; Whitaker, Weston R.; Till, Lisa; Grover, Madhusudan; Linden, David R.; Akiba, Yasutada; Kandimalla, Karunya K.; Zachos, Nicholas C.; Kaunitz, Jonathan D. (2018-06-13). "Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion". Cell Host & Microbe. 23 (6): 775–785.e5. doi:10.1016/j.chom.2018.05.004. ISSN 1931-3128. PMC 6055526. PMID 29902441.
  46. ^ Field, Michael (2003). "Intestinal ion transport and the pathophysiology of diarrhea". Journal of Clinical Investigation. 111 (7): 931–943. doi:10.1172/JCI200318326. ISSN 0021-9738. PMC 152597. PMID 12671039.
  47. ^ "Microbiome-Lax May Relieve Constipation". GEN - Genetic Engineering and Biotechnology News. 2018-06-15. Retrieved 2020-12-11.
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