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.