Fig. 8.
Chronic fluoxetine treatment enhances presynaptic 5-HT1BR-mediated reduction of the pause of the spontaneous firing in SNr GABA neurons. A: example traces showing the pausing effect of striatonigral IPSPs in a SNr GABA neuron before (A1), during (A2), and after (A3) bath application of 0.1 μM CP93129 in a saline-treated control mouse. B: example traces showing the pausing effect of striatonigral IPSPs on the firing of a SNr GABA neuron before (B1), during (B2), and after (B3) bath application of 0.1 μM CP93129 in a chronic fluoxetine-treated mouse. Horizontal bars in A1 and B1 indicate the pause duration: the time window between the stimulus artifact and the first spike after the stimulus artifact in each sweep. C: pooled data showing that 0.1 μM CP93129 reduced the pause duration to a larger extent in chronic fluoxetine-treated mice than in saline-treated mice. D: pooled data showing that 0.1 μM CP93129 reduced the peak amplitude of the striatonigral IPSPs more strongly in chronic fluoxetine-treated mice than in saline-treated mice (n = 6 neurons from 6 slices of 5 fluoxetine-treated mice; n = 7 neurons from 7 slices of 6 saline-treated mice).