Fig. 3.

Properties of evoked GABA currents in KC somata. A: brief pressure application of GABA (100 μM) to a recorded KC [K-gluconate-based intracellular solution (K-gluc. int. soln.), V_h = −73 mV] evokes a transient inward current that is inhibited by PTX (example currents show the average of 4 consecutive responses evoked at 30-s intervals). B: pooled data (n = 4) showing that GABA-evoked responses are insensitive to the GABA_A receptor antagonist bicuculline (50 μM) and the GABA_C receptor antagonist TPMPA (100 μM). Bicuculline, TPMPA, and PTX were applied sequentially to the same KC recordings. C: example GABA responses evoked at different V_h (−73, −58, and −43 mV) and pooled data (n = 4) showing the reversal potential of GABA-evoked currents with K-gluc. int. soln. D: example responses showing the size and kinetics of GABA-evoked currents (100 ms and 1-s applications) recorded with CsCl int. soln. (V_h = −65 mV). E: an example response evoked by longer application of GABA (same KC recording as D) showing the time course of current desensitization. F: example response (average of 4 traces) showing that local application of l-glutamate evokes a small, slow response in KCs (CsCl int. soln., V_h = −65 mV; note difference in scale bar from D). G: pooled data showing the peak amplitude of KC responses evoked by local application of GABA (100 μM, n = 7) and l-glutamate (1 mM, n = 2). *P < 0.05, statistical significance.