title: Lateral entorhinal cortex lesions rearrange afferents, glutamate receptors, increase seizure latency and suppress seizure-induced c-fos expression in the hippocampus of adult rat.
abstract: The entorhinal cortex (EC) provides the predominant excitatory drive to the hippocampal CA1 and subicular neurones in chronic epilepsy. Here we analysed the effects of one-sided lateral EC (LEC) and temporoammonic (alvear) path lesion on the development and properties of 4-aminopyridine-induced seizures. Electroencephalography (EEG) analysis of freely moving rats identified that the lesion increased the latency of the hippocampal seizure significantly and decreased the number of brief convulsions. Seizure-induced neuronal c-fos expression was reduced in every hippocampal area following LEC lesion. Immunocytochemical analysis 40 days after the ablation of the LEC identified sprouting of cholinergic and calretinin-containing axons into the dentate molecular layer. Region and subunit specific changes in the expression of ionotropic glutamate receptors (iGluRs) were identified. Although the total amount of AMPA receptor subunits remained unchanged, GluR1(flop) displayed a significant decrease in the CA1 region. An increase in NR1 and NR2B N-methyl-d-aspartate (NMDA) receptor subunits and KA-2 kainate receptor subunit was identified in the deafferented layers of the hippocampus. These results further emphasize the importance of the lateral entorhinal area in the spread and regulation of hippocampal seizures and highlight the potential role of the rewiring of afferents and rearrangement of iGluRs in the dentate gyrus in hippocampal convulsive activity.
authors.affiliation: Department of Neurosurgery, Faculty of Medicine, University of Szeged, Szeged, Hungary.
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Kopniczky
authors.forename: Endre
authors.initials: E
authors.lastname: Dobó
authors.forename: Sándor
authors.initials: S
authors.lastname: Borbély
authors.forename: Ildikó
authors.initials: I
authors.lastname: Világi
authors.forename: László
authors.initials: L
authors.lastname: Détári
authors.forename: Beáta
authors.initials: B
authors.lastname: Krisztin-Péva
authors.forename: Andrea
authors.initials: A
authors.lastname: Bagosi
authors.forename: Elek
authors.initials: E
authors.lastname: Molnár
authors.forename: András
authors.initials: A
authors.lastname: Mihály
mesh_terms: D015761:4-Aminopyridine; D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D001927:Brain Diseases / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D004198:Disease Susceptibility; D004569:Electroencephalography; D004594:Electrophysiology / Q000379:methods; D018728:Entorhinal Cortex / Q000473:pathology / Q000503:physiopathology*; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D009473:Neuronal Plasticity; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time; D017470:Receptors, Glutamate / Q000378:metabolism*; D012640:Seizures / Q000139:chemically induced / Q000503:physiopathology*
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D017470:Receptors, Glutamate; D015761:4-Aminopyridine