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Title: Changes of K+-Cl- cotransporter 2 (KCC2) and circuit activity in propofol-induced impairment of long-term potentiation in rat hippocampal slices
Author: null(王 伟) ; Wang, Hao ; Gong, Neng ; Xu, Tian-Le(徐天乐)
Source: BRAIN RESEARCH BULLETIN
Issued Date: 2006
Volume: 70, Issue:41005, Pages:444-449
Keyword: long-term potentiation ; learning and memory ; KCC2 ; propofol ; hippocampus ; DOWN-REGULATION ; NEURONS ; ANESTHESIA ; MECHANISM ; LTP ; EXCITABILITY ; EXPRESSION ; DEPRESSION ; RECEPTORS ; CHLORIDE
Subject: Neurosciences & Neurology
Corresponding Author: 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
English Abstract: 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.
Indexed Type: SCI
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/1802
Appears in Collections:神经所(总)_期刊论文
视知觉机制研究组_期刊论文

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Wang, Wei; Wang, Hao; Gong, Neng; Xu, Tian-Le.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,2006,70(41005):444-449
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