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Titolo:
Kainate receptors regulate unitary IPSCs elicited in pyramidal cells by fast-spiking interneurons in the neocortex
Autore:
Ali, AB; Rossier, J; Staiger, JF; Audinat, E;
Indirizzi:
Ecole Super Phys & Chim Ind, Lab Neurobiol & Divers Cellulaire, CNRS, UMR 7637, F-75231 Paris 5, France Ecole Super Phys & Chim Ind Paris France 5 7637, F-75231 Paris 5, France Univ Dusseldorf, D-40001 Dusseldorf, Germany Univ Dusseldorf Dusseldorf Germany D-40001 , D-40001 Dusseldorf, Germany O Vogt Inst Brain Res, D-40001 Dusseldorf, Germany O Vogt Inst Brain Res Dusseldorf Germany D-40001 001 Dusseldorf, Germany
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 9, volume: 21, anno: 2001,
pagine: 2992 - 2999
SICI:
0270-6474(20010501)21:9<2992:KRRUIE>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED EPILEPTIFORM ACTIVITY; RAT HIPPOCAMPAL SLICE; SYNAPTIC TRANSMISSION; GABA RELEASE; INHIBITION; NEURONS; GLUTAMATE; SYNAPSES; ACTIVATION; MECHANISMS;
Keywords:
GYKI; kainate receptors; ATPA; neocortical pyramidal cells; neocortical fast spiking interneurons; IPSC; EPSC;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Ali, AB Univ Oxford, Physiol Lab, Parks Rd, Oxford OX1 3PT, England Univ Oxford Parks Rd Oxford England OX1 3PT ford OX1 3PT, England
Citazione:
A.B. Ali et al., "Kainate receptors regulate unitary IPSCs elicited in pyramidal cells by fast-spiking interneurons in the neocortex", J NEUROSC, 21(9), 2001, pp. 2992-2999

Abstract

Unitary IPSCs elicited by fast-spiking (FS) interneurons in layer V pyramidal cells of the neocortex were studied by means of dual whole-cell recordings in acute slices. FS to pyramidal cell unitary IPSCs were depressed by (RS)-S-amino-3-(3-hydroxy-5-tertbutylisoxazol-4-yl) (ATPA), a kainate (KA) receptor agonist, and by the endogenous agonist L-glutamate in the presence of AMPA, NMDA, mGluR, and GABA(B) receptor antagonists. This effect was accompanied by an increase in failure rate of synaptic transmission, in the coefficient of variation, and in the paired pulse ratio, indicating a presynaptic origin of the IPSC depression. Pairing the activation of the presynaptic neuron with a depolarization of the postsynaptic cell mimicked the decrease of unitary IPSCs, and this effect persisted when postsynaptic sodium action potentials were blocked with the local anesthetic QX314. The effects of ATPA, glutamate, and of the pairing protocol were almost totally blocked by CNQX. These data suggest that KA receptors located on presynaptic FS cell terminals decrease the release of GABA and can be activated by glutamate released from the somatodendritic compartment of the postsynaptic pyramidalcells.

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Documento generato il 06/04/20 alle ore 07:29:22