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The Journal of Neuroscience, May 1, 2001, 21(9):2992-2999
Kainate Receptors Regulate Unitary IPSCs Elicited in Pyramidal Cells by Fast-Spiking Interneurons in the Neocortex
Afia B. Ali1, Jean Rossier1, Jochen F. Staiger2, and Etienne Audinat1 1 Laboratoire de Neurobiologie et Diversité Cellulaire, Centre National de la Recherche Scientifique, Unité Mixte Recherche 7637, ESPCI, 75231, Paris, Cedex 5, France, and 2 Heinrich-Heine University, C. and O. Vogt Institute for Brain Research, D-40001 Düsseldorf, Germany
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-tert-butylisoxazol-4-yl) (ATPA), a kainate (KA) receptor agonist, and by the endogenous agonist L-glutamate in the presence of AMPA, NMDA, mGluR, and GABAB 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 pyramidal cells.
Key words: GYKI; kainate receptors; ATPA; neocortical pyramidal cells; neocortical fast spiking interneurons; IPSC; EPSC
Copyright © 2001 Society for Neuroscience 0270-6474/01/2192992-08$05.00/0
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