Figure 4.

GABAergic Inhibition Is Responsible for SHs in L2/3Ps of V1

(A) Changes in excitatory (Ge, green) and inhibitory (Gi, red) conductances evoked by sound in a V1 L2/3P. Top: V_m responses under different current injections (from top: 100 pA, 0 pA, −100 pA). Middle: note the decrease of membrane resistance (R) during the SH. Bottom: time courses of the changes of G_e and G_i.

(B) Examples and box plots of subthreshold acoustic responses in controls (black) and during intracellular perfusion with 1 mM PTX/Cs (red). This manipulation significantly counteracted SHs (^∗∗p < 0.01).

(C) Examples, grand-averages (left) and amplitudes (right plots) of subthreshold responses to sound measured within 150 ms (top plot) and between 150 and 400 ms (bottom plot) poststimulus in the presence of GABA_A (gabazine 1.5 μM, green, n = 8), GABA_B (CGP52432 1 μM, red; n = 15) antagonists or both (blue; n = 6). Gabazine and CGP52432 effectively counteracted SHs in the early (^∗∗∗p < 0.001, for post hoc test) and late (^∗∗p < 0.01, for post hoc test) time windows, respectively.

(D and E) Effects of GABA_A and GABA_B antagonists on SH kinetics. Onset latencies (D) and half-widths (E) of SHs under GABA_A (green) or GABA_B (red) antagonists. (D) Gabazine significantly delayed the onset of SHs (^∗∗∗p < 0.001, for post hoc test). (E) Both gabazine and CGP52432 significantly shortened SHs (^∗∗∗p < 0.001, for post hoc test).

See also Figure S4.