AN EXPERIMENTAL-MODEL OF PROGRESSIVE EPILEPSY - THE DEVELOPMENT OF KINDLING OF THE HIPPOCAMPUS OF THE RAT
被引:26
作者:
DASILVA, LFH
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机构:Graduate School of Neurosciences Amsterdam, Institute of Neurobiology, University of Amsterdam, Amsterdam, 1098 SM
DASILVA, LFH
KAMPHUIS, W
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机构:Graduate School of Neurosciences Amsterdam, Institute of Neurobiology, University of Amsterdam, Amsterdam, 1098 SM
KAMPHUIS, W
TITULAER, M
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机构:Graduate School of Neurosciences Amsterdam, Institute of Neurobiology, University of Amsterdam, Amsterdam, 1098 SM
TITULAER, M
VREUGDENHIL, M
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机构:Graduate School of Neurosciences Amsterdam, Institute of Neurobiology, University of Amsterdam, Amsterdam, 1098 SM
VREUGDENHIL, M
WADMAN, WJ
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机构:Graduate School of Neurosciences Amsterdam, Institute of Neurobiology, University of Amsterdam, Amsterdam, 1098 SM
WADMAN, WJ
机构:
[1] Graduate School of Neurosciences Amsterdam, Institute of Neurobiology, University of Amsterdam, Amsterdam, 1098 SM
来源:
ITALIAN JOURNAL OF NEUROLOGICAL SCIENCES
|
1995年
/
16卷
/
1-2期
关键词:
KINDLING;
EPILEPSY;
HIPPOCAMPUS;
FIELD POTENTIALS;
INHIBITION;
GABA(A) RECEPTOR;
MESSENGER-RNA EXPRESSION;
IN SITU HYBRIDIZATION;
D O I:
10.1007/BF02229074
中图分类号:
R74 [神经病学与精神病学];
学科分类号:
摘要:
Kindling epileptogenesis was induced by periodic electrical stimulation of the Schaffer collateral/commissural pathway in the CAI area of the rat hippocampus, The progressive nature of hippocampal kindling is demonstrated by a detailed description of the behavioral signs and the progressive increase of the after-discharge duration in the course of kindling acquisition. Furthermore, the evolution of the alterations in the paired-pulse local evoked field potentials and the modifications of the GABA, receptor binding and of the expression of mRNAs encoding for the subunits of the GABA, and glutamate receptors are considered, Evidence is presented that during kindling opposite changes occur in the CAI and the fascia dentata in terms of the balance between excitation and inhibition due to contrasting changes in GABA-medicated inhibitory function.