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Titolo:
Epileptiform activity and EPSP-spike potentiation induced in rat hippocampal CA1 slices by repeated high-K+: involvement of ionotropic glutamate receptors and Ca2+/calmodulin-dependent protein kinase II
Autore:
Semyanov, A; Godukhin, O;
Indirizzi:
Russian Acad Sci, Inst Theoret & Expt Biophys, Pushchino 142292, Moscow Region, Russia Russian Acad Sci Pushchino Moscow Region Russia 142292 cow Region, Russia
Titolo Testata:
NEUROPHARMACOLOGY
fascicolo: 2, volume: 40, anno: 2001,
pagine: 203 - 211
SICI:
0028-3908(2001)40:2<203:EAAEPI>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; KINDLING-LIKE STATE; PYRAMIDAL NEURONS; CA2+ CHANNELS; NMDA RECEPTOR; CALMODULIN; INHIBITOR; EPILEPSY; SEIZURES; MODEL;
Keywords:
hippocampal CA1 slices; field potentials; epileptiform activity; EPSP-spike potentiation; NMDA glutamate receptor; Ca2+/calmodulin-dependent protein kinase II;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Godukhin, O Russian Acad Sci, Inst Theoret & Expt Biophys, Pushchino 142292, Moscow Region, Russia Russian Acad Sci Pushchino Moscow Region Russia 142292 Russia
Citazione:
A. Semyanov e O. Godukhin, "Epileptiform activity and EPSP-spike potentiation induced in rat hippocampal CA1 slices by repeated high-K+: involvement of ionotropic glutamate receptors and Ca2+/calmodulin-dependent protein kinase II", NEUROPHARM, 40(2), 2001, pp. 203-211

Abstract

We have previously demonstrated that repeated brief increases in extracellular K+ (K-o(+)) induce a hyperexcitability in CA1 pyramidal cells that persists for a long time after the final application of K+ [Neurosci. Lett. 223 (1997) 177; Epilepsy Research (2000) 75]. This epileptiform activity, which was associated with a lasting excitatory postsynaptic potential (EPSP)-spike potentiation, presented some of the characteristic features of traditional in vivo kindling. We have also found that Ca2+ influx through L-type voltage-sensitive Ca2+ channels is essential for the development of both in vitro kindling and EPSP-spike potentiation. The aims of this study were to investigate the involvement of ionotropic glutamate receptors, especially those of the NMDA subtype, and the requirement for Ca2+/calmodulin-dependentprotein kinase II (CaMKII) in these phenomena. Field EPSPs with presynaptic fibre volleys from the stratum radiatum, and population spikes from the stratum pyramidale, were recorded in the CA1 area of rat hippocampal slices in response to electrical stimulation of the Schaffer collateral/commissural fibres. Repeated (three episodes) brief (30 s) increases in extracellularK+ induced a sustained decrease in the threshold for development of evokedepileptiform discharges (i.e. an in vitro kindling-like state) and a lasting potentiation of the EPSP-spike transfer in CA1 pyramidal neurons (EPSP-spike potentiation). The selective antagonist of NMDA receptors, APV (50 muM), blocked the EPSP-spike potentiation, depressed the induction phase of the in vitro kindling-like state, and blocked the maintenance phase of this state. In contrast to APV, the blockade of AMPA/kainate receptors by CNQX (10 muM) had no effect. Like APV, KN62 (3 muM), a selective membrane permeable inhibitor of CaMKII, blocked the EPSP-spike potentiation and the maintenance phase of the in vitro kindling-like state. Our previous and present results therefore demonstrate that Ca2+ influxes through L-type voltage-dependent-and NMDA receptor-dependent-Ca2+ channels contribute differentially to the development of an in vitro kindling-like state, and both induce EPSP-spike potentiation in CA1 hippocampal pyramidal cells in response to repeatedbrief increases in K-o(+). It is suggested that these effects of intracellular Ca2+ on the maintenance phase of the in vitro kindling-like state and EPSP-spike potentiation are mediated by CaMKII-dependent mechanisms. (C) 2000 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 15:53:32