Previous research in our lab indicated that kainate receptors are inhibited by acute ethanol (Lack et al., 2008). These results suggested that KA-Rs might then be up-regulated during chronic intermittent exposure and withdrawal in response to this acute sensitivity. Therefore, we determined the contribution made by KA-Rs to glutamatergic synaptic responses during CIE and WD. To examine this, we used electrophysiology to measure the input/output (stimulus-response) relationship for KA-R via stimulation of the external capsule (Li et al., 2001; Li and Rogawski, 1998). Since KA-R mediated responses are small relative to AMPA-mediate synaptic currents, we measured evoked kainate EPSCs using stimulus trains of 3 pulses (100Hz, 10msec inter-stimulus interval) in the presence of a blocker cocktail containing the NMDA receptor antagonist APV, the GABAA receptor antagonist bicuculline, and the non-competitive AMPA receptor antagonist GYKI 53655 (Fig. 1A, C).
