Figure 4.

Activation of postsynaptic T-type Ca²⁺ channels is required for GABA_A-mediated burst firing. A, Top, Synaptically evoked action potentials in a TRN neuron recorded in cell-attached mode (left), blocked by application of the specific T-type Ca²⁺ channel blocker TTA-P2 (1 μm; right). Bottom, Raster plot showing the timing of spikes in the same neuron evoked by single stimuli applied at t = 0 ms, before and during bath application of TTA-P2 (1 μm). B, Summary data showing the time course of the TTA-P2-induced block in synaptically evoked action potential firing in TRN neurons (n = 5 neurons). C, A representative recording in cell-attached current-clamp mode showing that TTA-P2 (1 μm) blocked burst firing and reduced stimulus-induced membrane depolarization with the remaining component blocked by gabazine (10 μm). Identical results were obtained for four other neurons. D, Time course of the synaptically evoked depolarization (measured as area underneath the recording trace for the first 100 ms, normalized to control) during wash-in of TTA-P2 (1 μm) and gabazine (10 μm), for the same cell shown in C. E, A representative experiment showing that TTA-P2 (1 μm) had no effect on GABAergic PSC amplitude or paired-pulse plasticity. TRN neurons were recorded in whole-cell voltage clamp and intra-TRN GABAergic synapses were activated with paired pulses (20 Hz). Traces are averaged over 20–30 individual trials. F, Summary plot showing that bath application of TTA-P2 (1 μm) did not influence GABAergic PSC amplitude or paired-pulse ratio (PSC₂/PSC₁) (n = 5; p = 0.71 for amplitude; p = 0.72 for PPR; paired Student's t test). AMP, Amplitude; PPR, paired-pulse ratio.