Fig. S5.
Properties of LTPGABA. (A) IPSPs generated by a single pulse delivered to the GoC axon in the presence of NBQX. GrCs were injected with a constant depolarizing current to reach the membrane potential of −55 mV (−53.9 ± 1.1 mV, average injected current 4.5 ± 1.4 pA, n = 10). This value was chosen to increase the driving force of Cl− based GABAergic currents while avoiding the activation of NMDA currents. (Upper) Average IPSPs obtained before (black) and after (gray) the induction of LTPGABA. Histogram shows the effect of LTPGABA on peak amplitude (46.1 ± 6.4%, **P < 0.01, n = 5), time to peak (30.2 ± 4.2%, n = 5, **P < 0.01), and total depolarization (28.3 ± 3.4%, **P < 0.01, n = 5). (Lower) Average IPSPs obtained before (black) and after (gray) the induction of LTDGABA. Histogram shows the effect of LTDGABA on peak amplitude (−24.5 ± 2.8%, **P < 0.01, n = 5), time to peak (−10.6 ± 2.4%, n = 5, **P < 0.01), and total depolarization (12.7 ± 1.8%, **P < 0.01, n = 5). (B) Correlation of holding membrane potential with eIPSC peak amplitude normalized to maximum currents. LTPGABA and LTPGABA did not affect Cl− reversal potential. (CTR, black line, −71.4 ± 0.6 mV; LTPGABA dashed line, −71.3 ± 0.5 mV, n = 4; and LTDGABA gray line, −71.9 ± 0.8 mV n = 4). (C) Time course of spike-related parameters as in Fig. 1 obtained in the presence of d-APV to block GABAergic plasticity. (D) Time course of EPSP-related parameters as in Fig. 1 obtained in the presence of d-APV to block GABAergic plasticity.