Figure 11.

GABA_A receptor-mediated inhibition shunts the effect of HCN channels on excitatory synaptic integration. A1, 2PLSM image of a STN neuron together with sites of 2PLU of MNI-glutamate (green). A2, Somatic compound EPSPs generated by 2PLU of MNI-glutamate (green) during the injection of a 12 nS GABA_A receptor-mediated conductance under control conditions (black) and in the presence of ZD7288 (red). In the presence of the GABA_A conductance, blockade of HCN channels had little effect on the compound EPSP integral either in the example or the sample (A3; cells denoted by distinct colors; mean and SD indicated). B–D, Integration of three excitatory synaptic conductances (AMPA, 1 nS; NMDA, 5 nS) delivered to the distal dendritic compartment at 50 ms intervals was analyzed for each STN model under three regimes of inhibition. B, Somatic hyperpolarizing current was injected to generate to steady-state somatic hyperpolarization of −80 mV in each model (somatic, −57.9 pA; somatodendritic, −49.1 pA; deficient, −20.2 pA). C, Somatic GABAergic conductances (somatic, 14.5 nS; somatodendritic, 12.3 nS; deficient, 5.05 nS) were injected to generate steady-state somatic hyperpolarization of −80 mV. D, An identical somatic GABAergic conductance (12.3 nS) was injected for each model. When the GABAergic conductance was identical EPSP integration was not affected by the presence or absence of HCN channels although V_m was more hyperpolarized in the deficient model. Vm, Membrane potential.