Figure 6.

GABA-induced burst firing in TRN mediates long-latency inhibition in VB. VB thalamic neurons were recorded in the presence of blockers of excitatory neurotransmission, using a Cs-based internal solution. Cells were held at 0 mV. IPSCs were evoked with single stimuli, using stimulus electrodes placed in the TRN. A, B, Bath application of subsaturating concentrations of gabazine (0.2 μm) partially reduced short-latency IPSCs but completely eliminated long-latency IPSCs. A, Multiple trials are shown, recorded in control conditions and following wash-in of gabazine (0.2 μm). B, Time course of the IPSC integral (measured as the area underneath the current trace, normalized to baseline) for both short- (open circles) and long-latency responses (filled circles) during wash-in of gabazine (0.2 μm). The neuron is the same as in A. C, D, Bath application of WIN55,212 (WIN) (5 μm) reduced the amplitude of short-latency IPSCs but completely eliminated the long-latency IPSCs. C, Multiple trials are shown, recorded in control conditions and following bath application of WIN (5 μm). D, Time course of IPSC integral of short- (open circles) and long-latency responses (filled circles) during wash-in of WIN. The neuron is the same as in C. E, F, Pharmacological block of T-type Ca²⁺ channels by application of TTA-P2 (1 μm) eliminated the long-latency IPSC but did not influence short-latency IPSC. E, Multiple trials are shown, recorded in control conditions and following bath application of TTA-P2 (1 μm). F, Time course of IPSC integral for short- (open circles) and long-latency responses (filled circles). The neuron is the same as in E. G, Summary plot quantifying the effect of gabazine (10 μm; n = 5), low concentrations of gabazine (0.2 μm, n = 5), the CB1 receptor agonist WIN (n = 5), and TTA-P2 (n = 5) on short- (open bars) and long-latency IPSCs (gray bars). Error bars indicate SEM. H, Schematic illustrating TRN neuronal circuit mediating short- and long-latency IPSCs in VB neurons. Lat., Latency.