Blockade of ventral pallidum glutamatergic inputs restored DA neuron activity after long-term-abstinence from chronic cocaine.
The ventral pallidum (VP) attenuates VTA DA neuron population activity (Floresco et al., 2001), receives glutamatergic inputs from the BLA (Maslowski-Cobuzzi and Napier, 1994), and blocking glutamatergic inputs in the VP using kynurenic acid has been shown to restore DA population activity in the CMS model of depression (Chang and Grace, 2014). We used kynurenic acid, a broad-spectrum glutamate receptor antagonist (Floresco et al., 2001; Chang and Grace, 2014) to block glutamatergic afferents from the BLA to the VP. A representative example of placement of the infusion cannula is presented figure 5A, and the location of the vehicle and kynurenic acid (KYN) infusion cannula is presented figure 5B. Cocaine rats infused with vehicle (VEH) after 26-45 days abstinence had fewer spontaneously active DA neurons, in comparison to when VP glutamatergic inputs were blocked by kynurenic acid (Figure 5C left). No differences in the mean firing rate (figure 5C middle) or the percentage of spikes in a burst (figure 5C right) were observed.