期刊
NEUROSCIENCE
卷 146, 期 1, 页码 340-349出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2007.01.037
关键词
alcohol; ethanol; tolerance; desensitization; allostasis
资金
- NIAAA NIH HHS [AA12951, R01 AA012951] Funding Source: Medline
- NIA NIH HHS [AG18434, R01 AG018434] Funding Source: Medline
- NIDDK NIH HHS [P30 DK056341, DK56341, P30 DK056341-06] Funding Source: Medline
To determine how acute ethanol intoxication may alter memory processing, we examined the effects of stepwise increases in ethanol on long-term potentiation (LTP) in rat hippocampal slices. LTP was inhibited by acute administration of 60 mM ethanol, but was readily induced if ethanol was increased gradually to 60 mM over 75 min. Administration of 2-amino-5 phosphonovalerate (APV), an N-methyl-D-aspartate receptor (NMDAR) antagonist, during the stepwise increase in ethanol inhibited LTP, suggesting involvement of NMDARs in the development of tolerance. However, APV and nifedipine, an inhibitor of L-type calcium channels, failed to inhibit LTP when administered following the slow increase in ethanol. Ethanol-tolerant LTP was inhibited by thapsigargin, suggesting a major role for intracellular calcium release in this form of plasticity. The unique properties of ethanol-tolerant LTP suggest that memories formed during binge drinking are not acquired by standard synaptic mechanisms and that acute tolerance may involve the induction of novel mechanisms to maintain function. (C) 2007 IBRO. Published by Elsevier Ltd. All rights reserved.
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