Locally-generated acetaldehyde is involved in ethanol-mediated LTP inhibition in the hippocampus.
Kazuhiro Tokuda, Yukitoshi Izumi, Charles F Zorumski
文献索引:Neurosci. Lett. 537 , 40-3, (2013)
全文:HTML全文
摘要
Consistent with the ability of severe alcohol intoxication to impair memory, high concentrations of ethanol (60mM) acutely inhibit long-term potentiation (LTP) in the CA1 region of rat hippocampal slices. To account for this, we hypothesized that local metabolism to acetaldehyde may contribute to the effects of high ethanol on synaptic function. However, sodium azide, a catalase inhibitor, and allyl sulfide, an inhibitor of cytochrome P450 2E1 (CYP2E1), failed to overcome LTP inhibition by 60mM ethanol. In contrast, LTP was successfully induced in the presence of ethanol plus 4-methylpyrazole (4MP), an inhibitor of alcohol dehydrogenase, suggesting that local metabolism via alcohol dehydrogenase contributes to synaptic effects. Furthermore, exogenously administered acetaldehyde overcame the effects of 4MP on LTP inhibition mediated by ethanol. These observations indicate that acetaldehyde generated by local metabolism within the hippocampus participates in the synaptic dysfunction associated with severe alcohol intoxication.Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
相关化合物
相关文献:
2014-12-16
[Nucleic Acids Res. 42(22) , 14022-30, (2014)]
2014-10-01
[Biochim. Biophys. Acta 1838(10) , 2615-24, (2014)]
2015-01-01
[Drug Dev. Ind. Pharm. 41(1) , 156-62, (2014)]
2014-01-01
[PLoS ONE 9(11) , e112818, (2014)]
2015-03-01
[Tissue Eng. Part A 21(5-6) , 948-59, (2015)]