title: Synaptic responses in superficial layers of medial entorhinal cortex from rats with kainate-induced epilepsy.
abstract: 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 microM) 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.
authors.affiliation: Johannes-Müller-Institute of Physiology at the Charité, Humboldt University Berlin, Tucholskystr. 2, 10117 Berlin, Germany. else.tolner@helsinki.fi
authors.forename: Else A
authors.initials: EA
authors.lastname: Tolner
authors.forename: Christiane
authors.initials: C
authors.lastname: Frahm
authors.forename: Robert
authors.initials: R
authors.lastname: Metzger
authors.forename: Jan A
authors.initials: JA
authors.lastname: Gorter
authors.forename: Otto W
authors.initials: OW
authors.lastname: Witte
authors.forename: Fernando H
authors.initials: FH
authors.lastname: Lopes da Silva
authors.forename: Uwe
authors.initials: U
authors.lastname: Heinemann
mesh_terms: D000818:Animals; D003292:Convulsants; D004195:Disease Models, Animal; D004558:Electric Stimulation; D018728:Entorhinal Cortex / Q000503:physiopathology*; D004827:Epilepsy / Q000139:chemically induced / Q000503:physiopathology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D005968:Glutamate Decarboxylase / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D007395:Interneurons / Q000378:metabolism; D007527:Isoenzymes / Q000378:metabolism; D007608:Kainic Acid; D008297:Male; D009433:Neural Inhibition / Q000502:physiology; D009434:Neural Pathways / Q000503:physiopathology*; D009924:Organ Culture Techniques; D017729:Presynaptic Terminals / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D009435:Synaptic Transmission / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D003292:Convulsants; D018691:Excitatory Amino Acid Antagonists; D007527:Isoenzymes; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2; D007608:Kainic Acid