Synaptic responses in superficial layers of medial entorhinal cortex from rats with kainate-induced epilepsy

Neurobiology of Disease

Christiane Frahm¹  Robert Metzger²  Fernando H. Lopes da Silva²  Else A. Tolner³  Jan A. Gorter³  Uwe Heinemann⁴  Otto W. Witte⁴ 

[1] Corresponding author. Dept. of Biological and Environmental Sciences, University of Helsinki, P.O. Box 65 (Viikinkaari 1), 00014 Helsinki, Finland. Fax: [phone].;Department of Neurology, Friedrich-Schiller-University, Erlanger Allee 101, 07745 Jena, Germany;Johannes-Müller-Institute of Physiology at the Charité, Humboldt University Berlin, Tucholskystr. 2, 10117 Berlin, Germany;Swammerdam Institute of Life Sciences, Section of Neurobiology, University of Amsterdam, Graduate School of Neurosciences Amsterdam, NL-1098 SM, Amsterdam, The Netherlands;

关键词: Epileptogenesis;    Cell loss;    Presubiculum;    Disinhibition;    GAD65/67-hyperexcitability;   

DOI  :  

来源: DOAJ

【 摘 要 】

Mesial temporal lobe epilepsy patients often display shrinkage of the entorhinal cortex, which has been attributed to neuronal loss in medial entorhinal cortex layer III (MEC-III). MEC-III neuronal loss is reproduced in chronic epileptic rats after kainate-induced (KA) status epilepticus. Here we examined, in vitro, functional changes in superficial entorhinal cortex layers. Alterations in superficial layer circuitry were suggested by showing that presubiculum, parasubiculum and deep MEC stimulation evoked 100–300 Hz field potential transients and prolonged EPSPs (superimposed on IPSPs) in superficial MEC which were partially blocked by APV (in contrast to control) and fully blocked by CNQX. Contrary to controls, bicuculline (5 and 30 μM) had minor effects on evoked field potentials in KA rats. GAD65/67 in situ hybridization revealed preserved interneurons in MEC-III. In conclusion, hyperexcitability in superficial MEC neurons is not due to loss of GABAergic interneurons and probably results from alterations in synaptic connectivity within superficial MEC.

【 授权许可】

Unknown