Fig. 5
D2R upregulation is associated with reduced mPFC-evoked inhibition of ventral pallidal neurons in vivo. a, b Schematic depictions of the stimulating electrode in the medial prefrontal cortex (mPFC) and the recording electrode in the VP in anesthetized mice. mPFC stimulation can lead to excitation of VP neurons directly or via the subthalamic nucleus (STN). mPFC stimulation also leads to inhibitory responses in VP by activation of NAc GABAergic projection neurons. Solid green arrows and (+) sign depict excitatory projections, while the dotted red arrow and (–) sign represent inhibitory projections. Insets, representative VP spike waveforms from recorded cells (overlay of ~500 spikes; scale = 1.0 ms, 0.1 mV) are consistent with those of GABAergic neurons. We hypothesized that, in contrast to EGFP controls (a), additional D2Rs (pink) in NAc D2-MSNs would attenuate cortically-evoked inhibition of VP (b). c–f Z score transformed peristimulus time histograms (PSTHs) showing mPFC-evoked responses in all recorded VP neurons at different stimulation intensities. Electrical stimulation of the mPFC resulted in an excitation-inhibition response in the VP in the EGFPNAcInd mice. VP neurons in D2R-OENAcInd mice generally lacked the inhibitory response. g Change in firing rate during the 75 ms following mPFC stimulation expressed as a Z score of the pre-stimulation firing rate distribution. Basal firing rates were not different between the two groups (EGFPNAcInd mice: 8.83[1.67] Hz; D2R-OENAcInd mice: 11.18[2.08] Hz, t22 = −0.83, p = 0.42). EGFPNAcInd: n = 10 (5) units, D2R-OENAcInd: n = 14 (5) units. Error bars = s.e.m.
