Ab. 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
Unitary IPSCs elicited by fast-spiking (FS) interneurons in layer V pyramid
al cells of the neocortex were studied by means of dual whole-cell recordin
gs in acute slices. FS to pyramidal cell unitary IPSCs were depressed by (R
S)-S-amino-3-(3-hydroxy-5-tertbutylisoxazol-4-yl) (ATPA), a kainate (KA) re
ceptor agonist, and by the endogenous agonist L-glutamate in the presence o
f AMPA, NMDA, mGluR, and GABA(B) receptor antagonists. This effect was acco
mpanied by an increase in failure rate of synaptic transmission, in the coe
fficient of variation, and in the paired pulse ratio, indicating a presynap
tic origin of the IPSC depression. Pairing the activation of the presynapti
c neuron with a depolarization of the postsynaptic cell mimicked the decrea
se of unitary IPSCs, and this effect persisted when postsynaptic sodium act
ion potentials were blocked with the local anesthetic QX314. The effects of
ATPA, glutamate, and of the pairing protocol were almost totally blocked b
y CNQX. These data suggest that KA receptors located on presynaptic FS cell
terminals decrease the release of GABA and can be activated by glutamate r
eleased from the somatodendritic compartment of the postsynaptic pyramidal
cells.