Damage of hippocampal neurons in rats with chronic alcoholism

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Abstract

Chronic alcoholism can damage the cytoskeleton and aggravate neurological deficits. However, the effect of chronic alcoholism on hippocampal neurons remains unclear. In this study, a model of chronic alcoholism was established in rats that were fed with 6% alcohol for 42 days. Endogenous hydrogen sulfide content and cystathionine-beta-synthase activity in the hippocampus of rats with chronic alcoholism were significantly increased, while F-actin expression was decreased. Hippocampal neurons in rats with chronic alcoholism appeared to have a fuzzy nuclear membrane, mitochondrial edema, and ruptured mitochondrial crista. These findings suggest that chronic alcoholism can cause learning and memory decline in rats, which may be associated with the hydrogen sulfide/cystathionine-beta-synthase system, mitochondrial damage and reduced expression of F-actin.

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Most cited references 44

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The calpain system.

DARREL E. GOLL, VALERY THOMPSON, HONGQI LI … (2003)

The calpain system originally comprised three molecules: two Ca2+-dependent proteases, mu-calpain and m-calpain, and a third polypeptide, calpastatin, whose only known function is to inhibit the two calpains. Both mu- and m-calpain are heterodimers containing an identical 28-kDa subunit and an 80-kDa subunit that shares 55-65% sequence homology between the two proteases. The crystallographic structure of m-calpain reveals six "domains" in the 80-kDa subunit: 1). a 19-amino acid NH2-terminal sequence; 2). and 3). two domains that constitute the active site, IIa and IIb; 4). domain III; 5). an 18-amino acid extended sequence linking domain III to domain IV; and 6). domain IV, which resembles the penta EF-hand family of polypeptides. The single calpastatin gene can produce eight or more calpastatin polypeptides ranging from 17 to 85 kDa by use of different promoters and alternative splicing events. The physiological significance of these different calpastatins is unclear, although all bind to three different places on the calpain molecule; binding to at least two of the sites is Ca2+ dependent. Since 1989, cDNA cloning has identified 12 additional mRNAs in mammals that encode polypeptides homologous to domains IIa and IIb of the 80-kDa subunit of mu- and m-calpain, and calpain-like mRNAs have been identified in other organisms. The molecules encoded by these mRNAs have not been isolated, so little is known about their properties. How calpain activity is regulated in cells is still unclear, but the calpains ostensibly participate in a variety of cellular processes including remodeling of cytoskeletal/membrane attachments, different signal transduction pathways, and apoptosis. Deregulated calpain activity following loss of Ca2+ homeostasis results in tissue damage in response to events such as myocardial infarcts, stroke, and brain trauma.

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The vasorelaxant effect of H(2)S as a novel endogenous gaseous K(ATP) channel opener.

W Zhao, J ZHANG, Y. Lu … (2001)

Hydrogen sulfide (H(2)S) has been traditionally viewed as a toxic gas. It is also, however, endogenously generated from cysteine metabolism. We attempted to assess the physiological role of H(2)S in the regulation of vascular contractility, the modulation of H(2)S production in vascular tissues, and the underlying mechanisms. Intravenous bolus injection of H(2)S transiently decreased blood pressure of rats by 12- 30 mmHg, which was antagonized by prior blockade of K(ATP) channels. H(2)S relaxed rat aortic tissues in vitro in a K(ATP) channel-dependent manner. In isolated vascular smooth muscle cells (SMCs), H(2)S directly increased K(ATP) channel currents and hyperpolarized membrane. The expression of H(2)S-generating enzyme was identified in vascular SMCs, but not in endothelium. The endogenous production of H(2)S from different vascular tissues was also directly measured with the abundant level in the order of tail artery, aorta and mesenteric artery. Most importantly, H(2)S production from vascular tissues was enhanced by nitric oxide. Our results demonstrate that H(2)S is an important endogenous vasoactive factor and the first identified gaseous opener of K(ATP) channels in vascular SMCs.

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The novel neuromodulator hydrogen sulfide: an endogenous peroxynitrite 'scavenger'?

John B. Wong, Philip Moore, Matthew Whiteman … (2004)

Hydrogen sulfide (H2S) is a well-known cytotoxic gas. Recently it has been shown to stimulate N-methyl-D-aspartate (NMDA) receptors to enhance long-term potentiation suggesting a novel neuromodulatory role in vivo. Endogenous levels of H2S in the brain are reported to range between 10 and 160 microm. Considerably lower H2S levels are reported in the brains of Alzheimer's disease (AD) patients, where levels of brain protein nitration (probably mediated by peroxynitrite) are markedly increased. Activation of NMDA receptors leads to intracellular tyrosine nitration by peroxynitrite. Because H2S and peroxynitrite are important mediators in brain function and disease, we investigated the effects of the H2S 'donor', sodium hydrogen sulfide (NaSH) on peroxynitrite-mediated damage to biomolecules and to cultured human SH-SY5Y cells. H2S significantly inhibited peroxynitrite-mediated tyrosine nitration and inactivation of alpha1-antiproteinase to a similar extent to reduced glutathione at each concentration tested (30-250 microm). H2S also inhibited peroxynitrite-induced cytotoxicity, intracellular protein nitration and protein oxidation in human neuroblastoma SH-SY5Y cells. These data suggest that H2S has the potential to act as an inhibitor of peroxynitrite-mediated processes in vivo and that the potential antioxidant action of H2S deserves further study, given that extracellular GSH levels in the brain are very low.

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Author and article information

Journal

Journal ID (nlm-ta): Neural Regen Res

Journal ID (iso-abbrev): Neural Regen Res

Journal ID (publisher-id): NRR

Title: Neural Regeneration Research

Publisher: Medknow Publications & Media Pvt Ltd (India )

ISSN (Print): 1673-5374

ISSN (Electronic): 1876-7958

Publication date (Print): 01 September 2014

Volume: 9

Issue: 17

Pages: 1610-1615

Affiliations

[1 ]Second Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan Province, China

[2 ]Department of Physiology and Neurobiology, Xinxiang Medical University, Xinxiang, Henan Province, China

[3 ]Department of Neurology, the Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan Province, China

[4 ]Henan Provincial Key Laboratory of Bio-psychiatry, Xinxiang, Henan Province, China

Author notes

Yinsheng Li and Ruiling Zhang equally contributed to this work.

Corresponding author: Yinsheng Li, Department of Physiology and Neurobiology, Xinxiang Medical University, Xinxiang 453003, Henan Province, China, 13462256118@ 123456126.com . Ruiling Zhang, Second Affiliated Hospital of Xinxiang Medical University, Xinxiang 453003, Henan Province, China; Department of Physiology and Neurobiology, Xinxiang Medical University, Xinxiang 453003, Henan Province, China; Henan Provincial Key Laboratory of Bio-psychiatry, Xinxiang 453003, Henan Province, China, zrlxx2fy@ 123456126.com .

Author contributions: All authors were responsible for designing the experiment, implementing the experiments and evaluating the study. Du AL wrote the manuscript. All authors approved the final version of the manuscript .

Article

Publisher ID: NRR-9-1610

DOI: 10.4103/1673-5374.141787

PMC ID: 4211203

SO-VID: 349f11e9-1e9d-4acc-8533-e4749943d4ca

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date accepted : 10 May 2014

Damage of hippocampal neurons in rats with chronic alcoholism

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Most cited references 44

The calpain system.

The vasorelaxant effect of H(2)S as a novel endogenous gaseous K(ATP) channel opener.

The novel neuromodulator hydrogen sulfide: an endogenous peroxynitrite 'scavenger'?

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