期刊
NEUROCHEMISTRY INTERNATIONAL
卷 57, 期 3, 页码 177-188出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2010.06.001
关键词
beta-Alanine; Neurotransmitter; Gamma-aminobutyric acid; Glutamate; Uracil; Epilepsy; Sleep
资金
- Nova Scotia Health Research Foundation
- Epilepsy Canada
- Canadian Institute of Health Research
This review discusses the role of beta-alanine as a neurotransmitter. beta-Alanine is structurally intermediate between a-amino acid (glycine, glutamate) and gamma-amino acid (GABA) neurotransmitters. In general, beta-alanine satisfies a number of the prerequisite classical criteria for being a neurotransmitter: beta-alanine occurs naturally in the CNS, is released by electrical stimulation through a Ca2+ dependent process, has binding sites, and inhibits neuronal excitability. beta-Alanine has 5 recognized receptor sites: glycine co-agonist site on the NMDA complex (strychnine-insensitive); glycine receptor site (strychnine sensitive); GABA-A receptor; GABA-C receptor; and blockade of GAT protein-mediated glial GABA uptake. Although beta-alanine binding has been identified throughout the hippocampus, limbic structures, and neocortex, unique beta-alaninergic neurons with no GABAergic properties remain unidentified, and it is impossible to discriminate between beta-alaninergic and GABAergic properties in the CNS. Nevertheless, a variety of data suggest that beta-alanine should be considered as a small molecule neurotransmitter and should join the ranks of the other amino acid neurotransmitters. These realizations open the door for a more comprehensive evaluation of beta-alanine's neurochemistry and for its exploitation as a platform for drug design. (C) 2010 Elsevier Ltd. All rights reserved.
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