Document Detail


Chronic stress enhances synaptic plasticity due to disinhibition in the anterior cingulate cortex and induces hyper-locomotion in mice.
MedLine Citation:
PMID:  20035774     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The anterior cingulate cortex (ACC) is involved in the pathophysiology of a variety of mental disorders, many of which are exacerbated by stress. There are few studies, however, of stress-induced modification of synaptic function in the ACC that is relevant to emotional behavior. We investigated the effects of chronic restraint stress (CRS) on behavior and synaptic function in layers II/III of the ACC in mice. The duration of field excitatory postsynaptic potentials (fEPSPs) was longer in CRS mice than in control mice. The frequency of miniature inhibitory postsynaptic currents (mIPSCs) recorded by whole-cell patch-clamping was reduced in CRS mice, while miniature excitatory postsynaptic currents (mEPSCs) remained unchanged. Paired-pulse ratios (PPRs) of the fEPSP and evoked EPSC were larger in CRS. There was no difference in NMDA component of evoked EPSCs between the groups. Both long-term potentiation (LTP) and long-term depression of fEPSP were larger in CRS mice than in control mice. The differences between the groups in fEPSP duration, PPRs and LTP level were not observed when the GABA(A) receptor was blocked by bicuculline. Compared to control mice, CRS mice exhibited hyper-locomotive activity in an open field test, while no difference was observed between the groups in anxiety-like behavior in a light/dark choice test. CRS mice displayed decreased freezing behavior in fear conditioning tests compared to control mice. These findings suggest that CRS facilitates synaptic plasticity in the ACC via increased excitability due to disinhibition of GABA(A) receptor signalling, which may underlie induction of behavioral hyper-locomotive activity after CRS.
Authors:
Hiroshi Ito; Masatoshi Nagano; Hidenori Suzuki; Takayuki Murakoshi
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-12-24
Journal Detail:
Title:  Neuropharmacology     Volume:  58     ISSN:  1873-7064     ISO Abbreviation:  Neuropharmacology     Publication Date:    2010 Mar-Apr
Date Detail:
Created Date:  2010-02-15     Completed Date:  2010-09-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0236217     Medline TA:  Neuropharmacology     Country:  England    
Other Details:
Languages:  eng     Pagination:  746-57     Citation Subset:  IM    
Copyright Information:
Copyright 2009 Elsevier Ltd. All rights reserved.
Affiliation:
Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo 153-8902, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cerebral Cortex / physiology
Chronic Disease
Excitatory Postsynaptic Potentials / physiology*
Gyrus Cinguli / physiology*
Hyperkinesis / etiology,  physiopathology*,  psychology
Male
Mice
Mice, Inbred C57BL
Motor Activity / physiology
Neural Inhibition / physiology*
Neuronal Plasticity / physiology*
Stress, Psychological / complications,  physiopathology*,  psychology

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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