Figure 5. Stress Promotes GABA-mediated Excitation of VTA GABA Neurons Ex Vivo.

A) VTA GABA neurons were recorded in a cell-attached configuration before and after electrical stimulation of GABA_A receptor inputs. To isolate GABA_A receptor inputs, AMPA, NMDA, and GABA_B receptors were inhibited with antagonists: DNQX, AP5 and CGP55845 respectively.

B) Representative GABA neuron recording from a control animal demonstrated decreased firing rate in response to stimulation of GABAergic input (black). Similar stimulation enhanced the firing rate of VTA GABA neurons from stressed animals (red). For display, the traces were filtered and stimulus artifacts were removed.

C) Mean changes in VTA GABA neuron firing rate from control (black) and stressed (red) rat slices following repetitive stimulation of synaptic GABA inputs. **Significantly different from the control by ANOVA with repeated measures, p < 0.01, n = 8–10 cells/group.

D) Representative VTA GABA neuron recording from a stressed rat demonstrated that in the presence of picrotoxin (upper) or acetazolamide (ACTZ, lower), repetitive stimulation of GABA inputs failed to increase the firing rate.

E) Normalized mean changes in the firing rates of VTA GABA neurons in response to stimulation for each treatment group. Values were averaged over 5 s immediately following termination of the stimulation. In controls, GABA_A receptor-mediated increase in the firing rate was observed after slice incubation with corticosterone (blue). Significantly different from the control by t-test (p < 0.05, *), n = 8–10 cells/group or (p < 0.01, **), n = 6–8 cells/group.