Figure 4. Stress Increases Ethanol-induced GABA Neuron Firing Rates Ex Vivo.
A) Spontaneous firing rate of VTA GABA neurons was measured using the cell-attached configuration, and the whole-cell configuration was used to identify GABA neurons electrophysiologically and histochemically upon termination of the recording.
B) VTA GABA neurons displayed fast spontaneous firing rates (> 7 Hz) and lack of Ih current.
C) Neurobiotin-labeled VTA neurons with these electrophysiological properties were immuno-negative for tyrosine hydroxylase (TH), consistent with a non-DA phenotype.
D) VTA GABA neurons from stressed rats (red) showed a greater increase in firing rate following ethanol application (grey horizontal bar) than did GABA neurons from the unstressed controls (black). **Significantly different from the control by ANOVA with repeated measures, p < 0.01, n = 9 cells/group.
E) Glutamatergic receptor antagonists (DNQX and AP5) did not prevent the enhanced firing rate of VTA GABA neurons from stressed animals in response to ethanol. **Significantly different from the control by ANOVA with repeated measures, p < 0.01, n = 6–7 cells/group.
F) GABAA receptor antagonist, picrotoxin, prevented the ethanol-induced increase of GABA neuron firing rates after stress (red), and the firing rate was similar to the unstressed controls (black), n = 7–12 cells/group. The basal firing of VTA GABA neurons was not significantly different between control and stress groups (before ethanol): 11.1 ± 1.4 Hz vs. 11.3 ± 1.3 Hz, p > 0.05, n = 9.