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Titolo:
Long-lasting increase in cellular excitability associated with the primingof LTP induction in rat hippocampus
Autore:
Cohen, AS; Coussens, CM; Raymond, CR; Abraham, WC;
Indirizzi:
Univ Otago, Dept Psychol, Dunedin, New Zealand Univ Otago Dunedin New Zealand tago, Dept Psychol, Dunedin, New Zealand Univ Otago, Neurosci Res Ctr, Dunedin, New Zealand Univ Otago Dunedin New Zealand , Neurosci Res Ctr, Dunedin, New Zealand
Titolo Testata:
JOURNAL OF NEUROPHYSIOLOGY
fascicolo: 6, volume: 82, anno: 1999,
pagine: 3139 - 3148
SICI:
0022-3077(199912)82:6<3139:LIICEA>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
METABOTROPIC GLUTAMATE RECEPTORS; CA1 PYRAMIDAL NEURONS; CURRENT I-AHP; TERM POTENTIATION; CYCLIC-AMP; SYNAPTIC PLASTICITY; PROTEIN-KINASE; AREA CA1; ACTIVATION; INVITRO;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Abraham, WC Univ Otago, Dept Psychol, Box 56, Dunedin, New Zealand Univ Otago Box 56 Dunedin New Zealand , Dunedin, New Zealand
Citazione:
A.S. Cohen et al., "Long-lasting increase in cellular excitability associated with the primingof LTP induction in rat hippocampus", J NEUROPHYS, 82(6), 1999, pp. 3139-3148

Abstract

The mechanisms underlying the facilitation (priming) of long-term potentiation (LTP) by prior activation of metabotropic glutamate receptors (mGluRs)were investigated in area CA1 of rat hippocampal slices. In particular, wefocused on whether a long-lasting increase in postsynaptic excitability could account for the facilitated LTP. Administration of the mGluR agonist 1S,3R-aminocyclopentanedicarboxylic acid (ACPD) produced rapid decreases in the amplitude of both the slow spike afterhyperpolarization (AHP(slow)) and spike frequency adaptation recorded intracellularly from CA1 pyramidal cells. These changes persisted after drug washout, showing only a slow decay over 20 min. ACPD also caused a leftward shift of the field EPSP-population spike relation and an overall increase in population spike amplitude, but this effect was not as persistent as the intracellularly measured alterationsin cell excitability. ACPD-treated cells showed increased spike dischargesduring LTP-inducing tetanic stimulation, and the amplitude of the AHP(slow) was negatively correlated with the degree of initial LTP induction. The beta-adrenergic agonist isoproterenol also caused excitability changes as recorded intracellularly, whereas in extracellular experiments it weakly primed the induction but not the persistence of LTP. ACPD primed both LTP measures. Isoproterenol administration during the tetanus occluded the priming effect of ACPD on initial LTP induction but not its effect on LTP persistence. We conclude that the persistent excitability changes elicited by ACPD contributes to the priming of LTP induction but that other ACPD-triggered mechanisms must account for the facilitated persistence of LTP in the priming paradigm.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 15:51:11