Contribution of the nucleus accumbens to cocaine-induced responses of ventral 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. Eighty-four percent (16/19) of the tested neurons displayed rate changes following cocaine administration. Fifty-three percent responded by increasing firing rate, with an EMAX of 217 +/- 26% of basal activity and an ED50 of 0.07 +/- 0.03 mg/kg. Neurons that responded with a rate decrease (26%) had an EMAX of 14.3 +/- 9.0% of basal control and an ED50 of 0.04 +/- 0.02 mg/kg. One neuron (5%) displayed a biphasic response pattern. Haloperidol (0.2 mg/kg) attenuated cocaine-induced effects in 90% of the tested neurons. Given the responsiveness of VP neurons to cocaine, the extensive innervation of the VP by the nucleus accumbens (NAC), and the importance of the NAC in regulating cocaine-induced effects, it is likely that NAC activity may affect VP responses to cocaine. To test this possibility, the influence of NAC on cocaine-induced VP activity was evaluated. Unilateral inactivation of the NAC with microinjections of procaine (40 mu g/2 mu l/2 min) did not alter the proportion of VP neurons responsive to subsequent systemic administration of cocaine (0.1, 1.0 mg/kg iv) or the EMAX for those neurons showing a rate decrease. However, for the population of neurons showing a cocaine-induced rate increase, intra-NAC procaine significantly enhanced EMAX to 392 +/- 74% of control. These data suggest that the ability of VP neurons to respond to iv cocaine is independent of the NAC. However, the magnitude of the cocaine-induced effect appears to be dependent on NAC influences.