World Library  
Flag as Inappropriate
Email this Article

Hemicholinium-3

Article Id: WHEBN0004939546
Reproduction Date:

Title: Hemicholinium-3  
Author: World Heritage Encyclopedia
Language: English
Subject: Choline transporter, Triethylcholine, Acetylcholine, Solanaceae, List of compounds with carbon number 24
Collection: Alcohols, Morpholines, Quaternary Ammonium Compounds
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Hemicholinium-3

Hemicholinium-3
Systematic (IUPAC) name
(2S,2'S)-2,2'-biphenyl-4,4'-diylbis(2-hydroxy-4,4-dimethylmorpholin-4-ium)
Identifiers
CAS Registry Number  Y
ATC code None
PubChem CID:
IUPHAR/BPS
ChemSpider  Y
ChEMBL  N
Synonyms 2-[4-[4-(2-hydroxy-4,4-dimethylmorpholin-4-ium-2-yl)phenyl]phenyl]-4,4-dimethylmorpholin-4-ium-2-ol
Chemical data
Formula C24H34N2O42+
Molecular mass 414.538 g/mol
 N   

Hemicholinium-3 (HC3), also known as hemicholine, is a drug which blocks the reuptake of choline by the high-affinity choline transporter (ChT; encoded in humans by the gene SLC5A7) at the presynapse. The reuptake of choline is the rate limiting step in the synthesis of acetylcholine; hence, hemicholinium-3 decreases the synthesis of acetylcholine. It is therefore classified as an indirect acetylcholine antagonist.[1]

Acetylcholine is synthesized from choline and a donated acetyl group from acetyl-CoA, by the action of choline acetyltransferase (ChAT). Thus, decreasing the amount of choline available to a neuron will decrease the amount of acetylcholine produced. Neurons affected by hemicholinium-3 must rely on the transport of choline from the soma (cell body), rather than relying on reuptake of choline from the synaptic cleft.

Effects

Hemicholinium-3 has no clinical use, but is frequently used as a research tool in animal and in vitro experiments. The clinical use is limited since it prevents uptake into the cell which is not a rate limiting factor under normal, physiological frequencies of activation. This type of inhibition only becomes apparent at excessively high firing rates, whereby the uptake of choline into the nerve terminal as a rate limiting factor becomes apparent.

Hemoicholinium-3 produces a decrease in acetylcholine content in the nerve terminal and as a consequence results in a decrease in acetylcholine transmission. Since acetylcholine normally binds to nicotinic and muscarinic receptors in synapses, a decrease in acetylcholine would cause a decrease in nicotinic and muscarinic pharmacology.

See also

References

  1. ^ Carlson, Neil R. (2007). Physiology of Behavior (9th ed.). Boston: Pearson Education, Inc. p. 117.  


This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and USA.gov, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for USA.gov and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
 
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
 
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.
 



Copyright © World Library Foundation. All rights reserved. eBooks from World eBook Library are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.