Kainate receptor-mediated synaptic transmissions in the adult rodent insular cortex.

Kainate (KA) receptors are expressed widely in the central nerves systems, and regulate both excitatory and inhibitory synaptic transmission. KA receptors play important roles in fear memory, anxiety and pain. However, little is known about their function in synaptic transmission in the insular cortex (IC), a critical region for taste, memory and pain. Here we show that KA receptors contribute to fast synaptic transmission in neurons in all layers of the IC using whole cell patch-clamp recordings. In the presence of a GABAA receptor antagonist picrotoxin, a NMDA receptor antagonist AP5 and a selective AMPA receptor antagonist GYKI 53655, KA receptor-mediated excitatory postsynaptic currents (KA EPSCs) was revealed. We found KA EPSCs are about 5-10% of AMPA/KA EPSCs in all layers of the adult mouse IC. Similar results were found in adult rat IC. KA-EPSCs had a significantly slower rise time course and decay time constant compared with AMPA receptor-mediated EPSCs. High frequency repetitive stimulations at 200 Hz significantly facilitated the summation of KA EPSCs. Additionally, genetic deletion of GluK1 or GluK2 subunit partially reduced postsynaptic KA EPSCs, and GluK2 KO mice with a selective GluK1 antagonist UBP302 could significantly reduce the KA EPSCs. These data suggest that both GluK1 and GluK2 play functional roles in the IC. Our study may provide the synaptic basis for the physiology and pathology of KA receptors in the IC-related functions.