CONTRIBUTION OF THE NUCLEUS-ACCUMBENS TO COCAINE-INDUCED RESPONSES OFVENTRAL PALLIDAL NEURONS

The present study characterized the responses of ventral pallidal (VP) neurons to intravenously (iv) administered cocaine (0.003, 0.01, 0.03 , 0.1, 0.3, and 1.0 mg/kg) in chloral hydrate-anesthetized rats. Eight y-four percent (16/19) of the tested neurons displayed rate changes fo llowing cocaine administration. Fifty-three percent responded by incre asing firing rate, with an E(MAX) of 217 +/- 26% of basal activity and an ED(50) of 0.07 +/- 0.03 mg/kg. Neurons that responded with a rate decrease (26%) had an E(MAX) of 14.3 +/- 9.0% of basal control and an ED(50) of 0.04 +/- 0.02 mg/kg. One neuron (5%) displayed a biphasic re sponse pattern. Haloperidol (0.2 mg/kg) attenuated cocaine-induced eff ects in 90% of the tested neurons. Given the responsiveness of VP neur ons to cocaine, the extensive innervation of the VP by the nucleus acc umbens (NAC), and the importance of the NAC in regulating cocaine-indu ced effects, it is Likely that NAC activity may affect VP responses to cocaine. To test this possibility, the influence of NAC on cocaine-in duced VP activity was evaluated. Unilateral inactivation of the NAC wi th microinjections of procaine (40 mu g/2 mu l/2 min) did not alter th e proportion of VP neurons responsive to subsequent systemic administr ation of cocaine (0.1, 1.0 mg/kg iv) or the E(MAX) for those neurons s howing a rate decrease. However, for the population of neurons showing a cocaine-induced rate increase, intra-NAC procaine significantly enh anced E(MAX) to 392 +/- 74% of control. These data suggest that the ab ility of VP neurons to respond to iv cocaine is independent of the NAC . However, the magnitude of the cocaine-induced effect appears to be d ependent on NAC influences. (C) 1996 Wiley-Liss, Inc.