Changes of K+-Cl- cotransporter 2 (KCC2) and circuit activity in propofol-induced impairment of long-term potentiation in rat hippocampal slices

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	Changes of K+-Cl- cotransporter 2 (KCC2) and circuit activity in propofol-induced impairment of long-term potentiation in rat hippocampal slices
	Wang, Wei
刊名	BRAIN RESEARCH BULLETIN
	2006
卷号	70 期号:41005 页码:444-449
关键词	long-term potentiation learning and memory KCC2 propofol hippocampus DOWN-REGULATION NEURONS ANESTHESIA MECHANISM LTP EXCITABILITY EXPRESSION DEPRESSION RECEPTORS CHLORIDE
ISSN号	0361-9230
通讯作者	Xu, TL (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Neurosci, 320 Yue Yang Rd, Shanghai 200031, Peoples R China,tlxu@ion.ac.cn
英文摘要	Enhancing inhibition via gamma-aminobutyric acid type A (GABA(A)) receptors contributes to anesthetic-induced impairment of long-term potentiation (LTP) of excitatory synaptic transmission, which may account for general anesthesia-associated memory impairment (amnesia). The neuron-specific K+-Cl- cotransporter 2 (KCC2) is necessary for fast synaptic inhibition via maintaining the low intracellular chloride concentration required for the hyperpolarizing actions of GABA via GABAA receptors. To explore a possible role of KCC2-dependent inhibition in anesthetic-induced impairment of LTP, we used field excitatory postsynaptic potentials (fEPSP) recording and immunoblotting to study the effect of propofol on LTP maintenance and KCC2 expression in CA1 region of rat hippocampal slices. We found that propofol (30 mu M) not only impaired LTP expression but also prevented LTP-accompanied downregulation of KCC2 without affecting the basal transmission of glutamatergic synapses. Moreover, the recurrent inhibition in hippocampal slices was enhanced by propofol. These propofol-induced effects were completely abolished by picrotoxin, a specific GABAA receptor-chloride channel blocker. Thus, enhancement of GABAergic inhibition and suppression of neuronal excitability may account for the sustained expression of KCC2 and the impairment of LTP by propofol. Together, this study supports a novel role for KCC2 in UP expression and gives hints to a molecular mechanism, by which anesthetics might cause impairment of LTP. (c) 2006 Elsevier Inc. All rights reserved.
学科主题	Neurosciences & Neurology
收录类别	SCI
语种	英语
公开日期	2012-07-23
内容类型	期刊论文
源URL	[http://ir.sibs.ac.cn/handle/331001/1802]
专题	上海神经科学研究所_神经所(总) 上海神经科学研究所_视知觉机制研究组
推荐引用方式 GB/T 7714	Wang, Wei. Changes of K+-Cl- cotransporter 2 (KCC2) and circuit activity in propofol-induced impairment of long-term potentiation in rat hippocampal slices[J]. BRAIN RESEARCH BULLETIN,2006,70(41005):444-449.
APA	Wang, Wei.(2006).Changes of K+-Cl- cotransporter 2 (KCC2) and circuit activity in propofol-induced impairment of long-term potentiation in rat hippocampal slices.BRAIN RESEARCH BULLETIN,70(41005),444-449.
MLA	Wang, Wei."Changes of K+-Cl- cotransporter 2 (KCC2) and circuit activity in propofol-induced impairment of long-term potentiation in rat hippocampal slices".BRAIN RESEARCH BULLETIN 70.41005(2006):444-449.