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Titolo:
Kainate receptors depress excitatory synaptic transmission at CA3 -> CA1 synapses in the hippocampus via a direct presynaptic action
Autore:
Frerking, M; Schmitz, D; Zhou, Q; Johansen, J; Nicoll, RA;
Indirizzi:
Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA94143 USA Univ Calif San Francisco San Francisco CA USA 94143 rancisco, CA94143 USA Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 9, volume: 21, anno: 2001,
pagine: 2958 - 2966
SICI:
0270-6474(20010501)21:9<2958:KRDEST>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT HIPPOCAMPUS; MEDIATED RESPONSES; PYRAMIDAL CELLS; INHIBITION; ACTIVATION; RELEASE; INTERNEURONS; MECHANISMS; CA1; ANTAGONISM;
Keywords:
domoate; kainate; metabotropic; presynaptic; hippocampus; CA1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Nicoll, RA Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA94143 USA Univ Calif San Francisco San Francisco CA USA 94143 A94143 USA
Citazione:
M. Frerking et al., "Kainate receptors depress excitatory synaptic transmission at CA3 -> CA1 synapses in the hippocampus via a direct presynaptic action", J NEUROSC, 21(9), 2001, pp. 2958-2966

Abstract

Kainate receptor activation depresses synaptic release of neurotransmitterat a number of synapses in the CNS. The mechanism underlying this depression is controversial, and both ionotropic and metabotropic mechanisms have been suggested. We report here that the AMPA/kainate receptor agonists domoate (DA) and kainate (KA) cause a presynaptic depression of glutamatergic transmission at CA3-->CA1 synapses in the hippocampus, which is not blocked by the AMPA receptor antagonist GYKI 53655 but is blocked by the AMPA/KA receptor antagonist CNQX. Neither a blockade of interneuronal discharge nor antagonists of several neuromodulators affect the depression, suggesting thatit is not the result of indirect excitation and subsequent release of a neuromodulator. Presynaptic depolarization, achieved via increasing extracellular K+, caused a depression of the presynaptic fiber volley and an increase in the frequency of miniature EPSCs. Neither effect was observed with DA,suggesting that DA does not depress transmission via a presynaptic depolarization. However, the effects of DA were abolished by the G-protein inhibitors N-ethylmaleimide and pertussis toxin. These results suggest that KA receptor activation depresses synaptic transmission at this synapse via a direct, presynaptic, metabotropic action.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/04/20 alle ore 01:51:55