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Titolo:
Alterations of hippocampal GABAergic system contribute to development of spontaneous recurrent seizures in the rat lithium-pilocarpine model of temporal lobe epilepsy
Autore:
Andre, V; Marescaux, C; Nehlig, A; Fritschy, JM;
Indirizzi:
Univ Strasbourg 1, Fac Med, INSERM, U398, F-67085 Strasbourg, France Univ Strasbourg 1 Strasbourg France F-67085 , F-67085 Strasbourg, France Univ Zurich, Inst Pharmacol & Toxicol, CH-8006 Zurich, Switzerland Univ Zurich Zurich Switzerland CH-8006 icol, CH-8006 Zurich, Switzerland
Titolo Testata:
HIPPOCAMPUS
fascicolo: 4, volume: 11, anno: 2001,
pagine: 452 - 468
SICI:
1050-9631(2001)11:4<452:AOHGSC>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED STATUS EPILEPTICUS; DENTATE GRANULE CELLS; GABA(A) RECEPTOR FUNCTION; CA1 PYRAMIDAL NEURONS; KAINATE-TREATED RATS; SYNAPTIC REORGANIZATION; MOSSY FIBERS; KAINIC ACID; ADULT RATS; INTRAHIPPOCAMPAL KAINATE;
Keywords:
GABA transporter; neuronal damage; calcium-binding proteins; interneurons; inhibitory neurotransmission; axonal sprouting;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
70
Recensione:
Indirizzi per estratti:
Indirizzo: Nehlig, A Univ Strasbourg 1, Fac Med, INSERM, U398, 11 Rue Humann, F-67085Strasbourg, France Univ Strasbourg 1 11 Rue Humann Strasbourg France F-67085 rance
Citazione:
V. Andre et al., "Alterations of hippocampal GABAergic system contribute to development of spontaneous recurrent seizures in the rat lithium-pilocarpine model of temporal lobe epilepsy", HIPPOCAMPUS, 11(4), 2001, pp. 452-468

Abstract

Reorganization of excitatory and inhibitory circuits in the hippocampal formation following seizure-induced neuronal loss has been proposed to underlie the development of chronic seizures in temporal lobe epilepsy (TLE). Here, we investigated whether specific morphological alterations of the GABAergic system can be related to the onset of spontaneous recurrent seizures (SRS) in the rat lithium-pilocarpine model of TLE. Immunohistochemical staining for markers of interneurons and their projections, including parvalbumin(PV), calretinin (CR), calbindin (CB), glutamic acid decarboxylase (GAD), and type I GABA transporter (GAT1), was performed in brain sections of ratstreated with lithium-pilocarpine and sacrificed after 24 h, during the silent phase (6 and 12 days), or after the onset of SRS (10-18 days after treatment). Semiquantitative analysis revealed a selective loss of interneuronsin the stratum oriens of CAI, associated with a reduction of GAT1 stainingin the stratum radiatum and stratum oriens. In contrast, interneurons in CA3 were largely preserved, although GAT1 staining was also reduced. These changes occurred within 6 days after treatment and were therefore insufficient. to cause SRS. In the dentate gyrus, extensive cell loss occurred in thehilus. The pericellular innervation of granule cells by PV-positive axons was markedly reduced, although the loss of PV-interneurons was only partial. Most strikingly, the density of GABAergic axons, positive for both GAD and GAT1, was dramatically increased in the inner molecular layer. This change emerged during the silent period, but was most marked in animals with SRS. Finally, supernumerary CB-positive neurons were detected in the hilus, selectively in rats with SRS. These findings suggest that alterations of GABAergic circuits occur early after lithium-pilocarpine-induced status epilepticus and contribute to epileptogenesis. in particular, the reorganization of GABAergic axons in the dentate gyrus might contribute to synchronize hyperexcitability induced by the interneuron loss during the silent period, leading to the onset of chronic seizures. Hippocampus 200 1;11.452-468. (C) 2001 Wiley-Liss, Inc.

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Documento generato il 19/01/20 alle ore 09:17:31