Network stability through homeostatic scaling of excitatory and inhibitory synapses following inactivity in CA3 of rat organotypic hippocampal slice cultures

被引:28
作者
Buckby, LE [1 ]
Jensen, TP [1 ]
Smith, PJE [1 ]
Empson, RM [1 ]
机构
[1] Univ London, Sch Biol Sci, Egham TW20 0EX, Surrey, England
基金
英国生物技术与生命科学研究理事会;
关键词
hippocampus; synapsin; 1; glutamate; VGLUT1; GABA; GABA-A receptor; NR1; GluR1; homeostatic plasticity; homeostatic scaling; EPSP; IPSP;
D O I
10.1016/j.mcn.2006.01.009
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Homeostatic plasticity is a phenomenon whereby synaptic strength is scaled in the context of the activity that the network receives. Here, we have analysed excitatory and inhibitory synapses in a model of homeostatic plasticity where rat organotypic hippocampal slice cultures were deprived of excitatory synaptic input by the NMDA and AMPA/KA glutamate receptor antagonists, AP5 and CNQX. We show that chronic excitatory synapse deprivation generates an excitable CA3 network where enhanced amplitude and frequency of spontaneous excitatory post-synaptic potentials were associated with increased glutamate receptor subunit expression and increased number and size of synapsin 1 and VGLUT1 positive puncta. Intact spontaneous inhibitory post-synaptic potentials coincided Nvith persistent expression of the GABA-A receptor alpha subunit and GAD65 and an enhancement of parvalbumin-positive puncta. In this model of homeostatic plasticity, scaling up of synaptic excitation and maintenance of fast synaptic inhibition promote an excitable, but stable, CA3 network. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:805 / 816
页数:12
相关论文
共 46 条
[1]   Homeostatic plasticity in hippocampal slice cultures involves changes in voltage-gated Na+ channel expression [J].
Aptowicz, CO ;
Kunkler, PE ;
Kraig, RP .
BRAIN RESEARCH, 2004, 998 (02) :155-163
[2]   Chronic blockade of glutamate receptors enhances presynaptic release and downregulates the interaction between synaptophysin-synaptobrevin-vesicle-associated membrane protein 2 [J].
Bacci, A ;
Coco, S ;
Pravettoni, E ;
Schenk, U ;
Armano, S ;
Frassoni, C ;
Verderio, C ;
De Camilli, P ;
Matteoli, M .
JOURNAL OF NEUROSCIENCE, 2001, 21 (17) :6588-6596
[3]   CNQX increases GABA-mediated synaptic transmission in the cerebellum by an AMPA/kainate receptor-independent mechanism [J].
Brickley, SG ;
Farrant, M ;
Swanson, GT ;
Cull-Candy, SG .
NEUROPHARMACOLOGY, 2001, 41 (06) :730-736
[4]   The Center for the Study of Biological Complexity at Virginia Commonwealth University [J].
Buck, GA .
CHEMISTRY & BIODIVERSITY, 2004, 1 (01) :7-9
[5]   Synaptic gain control and homeostasis [J].
Burrone, J ;
Murthy, VN .
CURRENT OPINION IN NEUROBIOLOGY, 2003, 13 (05) :560-567
[6]   Multiple forms of synaptic plasticity triggered by selective suppression of activity in individual neurons [J].
Burrone, J ;
O'Byrne, M ;
Murthy, VN .
NATURE, 2002, 420 (6914) :414-418
[7]  
Cannon W.B., 1939, WISDOM BODY, DOI DOI 10.1097/00000441-193907000-00031
[8]   Synapse-specific control of synaptic efficacy at the terminals of a single neuron [J].
Davis, GW ;
Goodman, CS .
NATURE, 1998, 392 (6671) :82-86
[9]   Maintaining the stability of neural function: A homeostatic hypothesis [J].
Davis, GW ;
Bezprozvanny, I .
ANNUAL REVIEW OF PHYSIOLOGY, 2001, 63 :847-869
[10]   Homeostatic scaling of vesicular glutamate and GABA transporter expression in rat neocortical circuits [J].
De Gois, S ;
Schäfer, MKH ;
Defamie, N ;
Chen, C ;
Ricci, A ;
Weihe, E ;
Varoqui, H ;
Erickson, JD .
JOURNAL OF NEUROSCIENCE, 2005, 25 (31) :7121-7133