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Contents

   



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1 See also  




2 References  













T-HCA






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From Wikipedia, the free encyclopedia
  

Not to be confused with Tetrahydrocannabinolic acid.
T-HCA
Clinical data
Other namestrans-4-hydroxycrotonic acid
ATC code
  • None
Identifiers

  • (2E)-4-hydroxybut-2-enoic acid

CAS Number
PubChem CID
ChemSpider
UNII
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
FormulaC4H6O3
Molar mass102.089 g·mol−1
3D model (JSmol)

  • O=C(O)\C=C\CO

  • InChI=1S/C4H6O3/c5-3-1-2-4(6)7/h1-2,5H,3H2,(H,6,7)/b2-1+ checkY

  • Key:RMQJECWPWQIIPW-OWOJBTEDSA-N checkY

 ☒NcheckY (what is this?)  (verify)

trans-4-Hydroxycrotonic acid (T-HCA), also known as γ-hydroxycrotonic acid (GHC), is an agent used in scientific research to study the GHB receptor.[1] It is an analogueofγ-hydroxybutyric acid (GHB), as well as an active metabolite of GHB.[2][3][4] Similarly to GHB, T-HCA has been found to be endogenous to the rat central nervous system, and as a metabolite of GHB, is almost certain to be endogenous to humans as well.[3][5] T-HCA binds to the high-affinity GHB receptor with 4-fold greater affinity than GHB itself,[6] where it acts as an agonist,[1][7] but does not bind to the low-affinity GHB binding site, the GABAB receptor.[3][8] Because of this, T-HCA does not produce sedation. T-HCA has been shown to cause receptor activation-evoked increases in extracellular glutamate concentrations, notably in the hippocampus.[8]

See also[edit]

References[edit]

  1. ^ a b Tunnicliff G, Cash CD (2 September 2003). Gamma-Hydroxybutyrate: Pharmacological and Functional Aspects. CRC Press. pp. 24, 104. ISBN 978-0-203-30099-2.
  • ^ Quang LS, Desai MC, Kraner JC, Shannon MW, Woolf AD, Maher TJ (June 2002). "Enzyme and receptor antagonists for preventing toxicity from the gamma-hydroxybutyric acid precursor 1,4-butanediol in CD-1 mice". Annals of the New York Academy of Sciences. 965 (1): 461–472. Bibcode:2002NYASA.965..461Q. doi:10.1111/j.1749-6632.2002.tb04187.x. PMID 12105121. S2CID 25644267.
  • ^ a b c Bourguignon JJ, Schoenfelder A, Schmitt M, Wermuth CG, Hechler V, Charlier B, Maitre M (May 1988). "Analogues of gamma-hydroxybutyric acid. Synthesis and binding studies". Journal of Medicinal Chemistry. 31 (5): 893–897. doi:10.1021/jm00400a001. PMID 3361576.
  • ^ Maher TJ (24 January 2012). "Amino Acid Neurotransmitters in the Central Nervous System". In Lemke TL, Williams DA (eds.). Foye's Principles of Medicinal Chemistry. Lippincott Williams & Wilkins. pp. 414–. ISBN 978-1-60913-345-0.
  • ^ Vayer P, Dessort D, Bourguignon JJ, Wermuth CG, Mandel P, Maitre M (July 1985). "Natural occurrence of trans-gamma hydroxycrotonic acid in rat brain". Biochemical Pharmacology. 34 (13): 2401–2404. doi:10.1016/0006-2952(85)90804-4. PMID 4015683.
  • ^ Wellendorph P, Høg S, Greenwood JR, de Lichtenberg A, Nielsen B, Frølund B, et al. (October 2005). "Novel cyclic gamma-hydroxybutyrate (GHB) analogs with high affinity and stereoselectivity of binding to GHB sites in rat brain". The Journal of Pharmacology and Experimental Therapeutics. 315 (1): 346–351. doi:10.1124/jpet.105.090472. PMID 16014570. S2CID 10332754.
  • ^ Patrylo PR (27 May 2009). "Epilepsy and Seizure Susceptibility in the Aging Brain". In Schwartzkron PD (ed.). Encyclopedia of Basic Epilepsy Research. Academic Press. pp. 44–. ISBN 978-0-12-373961-2.
  • ^ a b Castelli MP, Ferraro L, Mocci I, Carta F, Carai MA, Antonelli T, et al. (November 2003). "Selective gamma-hydroxybutyric acid receptor ligands increase extracellular glutamate in the hippocampus, but fail to activate G protein and to produce the sedative/hypnotic effect of gamma-hydroxybutyric acid". Journal of Neurochemistry. 87 (3): 722–732. doi:10.1046/j.1471-4159.2003.02037.x. PMID 14535954. S2CID 82175813.
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