Fig. 11.

Modulation of guinea-pig SNr GABA neuron firing rate by H₂O₂. (A) Spontaneous activity of a SNr GABA neuron under control conditions, in the presence of H₂O₂ (1.5 mM), and with flufenamic acid (FFA; 20 µM) in the continued presence of H₂O₂. (B) H₂O₂ causes an increase in SNr GABA neuron firing rate that is reversed by the TRP channel blocker FFA, with the resulting firing rate falling below control levels. (C) Depletion of endogenous H₂O₂ with catalase (Cat; 500 U/mL) results in a decrease in firing rate and an increase in the coefficient of variation indicating that basal H₂O₂ levels play a role in maintaining the tonic firing of SNr GABA neurons. (D) Spontaneous activity of another SNr GABA neuron under control conditions, in the presence of FFA, and with H₂O₂ in the continued presence of FFA. (E, F) Blockade of TRP channels with FFA causes a decrease in SNr GABA neuron firing rate. Addition of H₂O₂ when TRP channels are blocked results in a suppression of firing, indicating activation of a hyperpolarizing conductance by H₂O₂ (E). The H₂O₂-induced suppression of firing is prevented by the K_ATP channel blocker glibenclamide (Glib; 3µM) (F). *p < 0.05; **p < 0.01; ***p < 0.001. Modified from Lee et al., 2011 with permission.