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Designer receptors show role for ventral pallidum input to ventral tegmental area in cocaine seeking NATURE NEUROSCIENCE Mahler, S. V., Vazey, E. M., Beckley, J. T., Keistler, C. R., McGlinchey, E. M., Kaufling, J., Wilson, S. P., Deisseroth, K., Woodward, J. J., Aston-Jones, G. 2014; 17 (4): 577-U136

Abstract

The ventral pallidum is centrally positioned within mesocorticolimbic reward circuits, and its dense projection to the ventral tegmental area (VTA) regulates neuronal activity there. However, the ventral pallidum is a heterogeneous structure, and how this complexity affects its role within wider reward circuits is unclear. We found that projections to VTA from the rostral ventral pallidum (RVP), but not the caudal ventral pallidum (CVP), were robustly Fos activated during cue-induced reinstatement of cocaine seeking--a rat model of relapse in addiction. Moreover, designer receptor-mediated transient inactivation of RVP neurons, their terminals in VTA or functional connectivity between RVP and VTA dopamine neurons blocked the ability of drug-associated cues (but not a cocaine prime) to reinstate cocaine seeking. In contrast, CVP neuronal inhibition blocked cocaine-primed, but not cue-induced, reinstatement. This double dissociation in ventral pallidum subregional roles in drug seeking is likely to be important for understanding the mesocorticolimbic circuits underlying reward seeking and addiction.

View details for DOI 10.1038/nn.3664

View details for Web of Science ID 000333405300018

View details for PubMedID 24584054

View details for PubMedCentralID PMC3973180