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Titolo:
Differential actions of PKA and PKC in the regulation of glutamate releaseby group III mGluRs in the entorhinal cortex
Autore:
Evans, DI; Jones, RSG; Woodhall, G;
Indirizzi:
Univ Bristol, Sch Med Sci, Dept Physiol, Bristol BS8 1TD, Avon, England Univ Bristol Bristol Avon England BS8 1TD Bristol BS8 1TD, Avon, England
Titolo Testata:
JOURNAL OF NEUROPHYSIOLOGY
fascicolo: 2, volume: 85, anno: 2001,
pagine: 571 - 579
SICI:
0022-3077(200102)85:2<571:DAOPAP>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; PROTEIN-KINASE-C; NEONATAL RAT HIPPOCAMPUS; CYCLIC-AMP FORMATION; METABOTROPIC GLUTAMATE; SYNAPTIC TRANSMISSION; ADENYLATE-CYCLASE; PHORBOL ESTERS; PRESYNAPTIC ENHANCEMENT; TRANSMITTER RELEASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Woodhall, G Univ Bristol, Sch Med Sci, Dept Physiol, Bristol BS8 1TD, Avon, England Univ Bristol Bristol Avon England BS8 1TD 1TD, Avon, England
Citazione:
D.I. Evans et al., "Differential actions of PKA and PKC in the regulation of glutamate releaseby group III mGluRs in the entorhinal cortex", J NEUROPHYS, 85(2), 2001, pp. 571-579

Abstract

In a previous study we showed that activation of a presynaptically locatedmetabotropic glutamate receptor (mGluR) with pharmacological properties ofmGluR4a causes a facilitation of glutamate release in layer V of the rat entorhinal cortex (EC) in vitro. In the present study we have begun to investigate the intracellular coupling linking the receptor to transmitter release. We recorded spontaneous alpha -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-mediated excitatory postsynaptic currents (EPSCs) in the whole cell configuration of the patch-clamp technique, from visually identified neurons in layer V. Bath application of the protein kinase A (PKA) activator, forskolin, resulted in a marked facilitation of EPSC frequency, similar to that seen with the mGluR4a specific agonist, ACPT-1. Preincubation of slices with the PKA inhibitor H-89 abolished the effect of ACPT-1, as did preincubation with the adenylate cyclase inhibitor, SQ22536. Activationof protein kinase C (PKC) using phorbol 12 myristate 13-acetate (PMA) did not affect sEPSC frequency; however, it did abolish the facilitatory effectof ACPT-1 on glutamate release. A robust enhancement of EPSC frequency wasseen in response to bath application of the specific PKC inhibitor, GF 109203X. Both H-89 and the group III mGluR antagonist (RS)-alpha -cyclopropyl-4-phosphonophenylglycine (CPPG) abolished the effects of GF 109203X. These data suggest that in layer V of the EC, presynaptic group III mGluRs facilitate release via a positive coupling to adenylate cyclase and subsequent activation of PKA. We have also demonstrated that the PKC system tonically depresses transmitter release onto layer V cells of the EC and that an interaction between mGluR4a, PKA, and PKC may exist at these synapses.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 03:04:53