N-METHYL-D-ASPARTIC ACID-INDUCED LESIONS OF THE NUCLEUS-ACCUMBENS ANDOR VENTRAL PALLIDUM FAIL TO ATTENUATE LATERAL HYPOTHALAMIC SELF-STIMULATION REWARD/

The role of ventral striatum in the maintenance and transmission of a hypothalamic intracranial self-stimulation (ICSS) reward signal was in vestigated using the rate-frequency multiple-curve shift paradigm. The excitotoxin N-methyl-D-aspartic acid (NMDA) was bilaterally administe red into the nucleus accumbens (15 mu g per side), the ventral pallidu m (15 mu g per side) or the juncture between the two structures (20 mu g per side) creating three lesion groups. Both the nucleus accumbens (NAC) lesion group and the ventral pallidum (VP) lesion group displaye d substantial NMDA-induced damage which was generally restricted to th e intended limbic structure. The NMDA lesions in the third group displ ayed extensive damage to both the NAC and VP, as intended, but also ty pically diffused into adjacent medial structures. NMDA-induced lesions in all groups caused a suppression in motor/performance activity at a ll currents tested. Contrary to motor effects, reward efficacy was rel atively unaffected for the NAC and VP groups. The lack of reward effec ts may be due to plasticity of neuronal systems and redundancy of circ uit connections. However, this explanation is questionable given the f act that NMDA lesions which encompassed both the NAC and VP had little effect on reward efficacy. The above data suggests that the nucleus a ccumbens and the ventral pallidum are not critical for ICSS rewards st imulation and that hypothalamic ICSS reward signals are processed down stream from these limbic structures.