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Title: Hydrogen sulfide: Neurochemistry and neurobiology
Authors: Qu, K.
Lee, S.W. 
Bian, J.S. 
Low, C.-M. 
Wong, P.T.-H. 
Keywords: CNS
Cystathionine β-synthase
Hydrogen sulfide
Issue Date: 2008
Citation: Qu, K., Lee, S.W., Bian, J.S., Low, C.-M., Wong, P.T.-H. (2008). Hydrogen sulfide: Neurochemistry and neurobiology. Neurochemistry International 52 (1) : 155-165. ScholarBank@NUS Repository.
Abstract: Current evidence suggests that hydrogen sulfide (H2S) plays an important role in brain functions, probably acting as a neuromodulator as well as an intracellular messenger. In the mammalian CNS, H2S is formed from the amino acid cysteine by the action of cystathionine β-synthase (CBS) with serine (Ser) as the by-product. As CBS is a calcium and calmodulin dependent enzyme, the biosynthesis of H2S should be acutely controlled by the intracellular concentration of calcium. In addition, it is also regulated by S-adenosylmethionine which acts as an allosteric activator of CBS. H2S, as a sulfhydryl compound, has similar reducing properties as glutathione. In neurons, H2S stimulates the production of cAMP probably by direct activation of adenylyl cyclase and thus activate cAMP-dependent processes. In astrocytes, H2S increases intracellular calcium to an extent capable of inducing and propagating a "calcium wave", which is a form of calcium signaling among these cells. Possible physiological functions of H2S include potentiating long-term potentials through activation of the NMDA receptors, regulating the redox status, maintaining the excitatory/inhibitory balance in neurotransmission, and inhibiting oxidative damage through scavenging free radicals and reactive species. H2S is also involved in CNS pathologies such as stroke and Alzheimer's disease. In stroke, H2S appears to act as a mediator of ischemic injuries and thus inhibition of its production has been suggested to be a potential treatment approach in stroke therapy. © 2007 Elsevier Ltd. All rights reserved.
Source Title: Neurochemistry International
ISSN: 01970186
DOI: 10.1016/j.neuint.2007.05.016
Appears in Collections:Staff Publications

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