Decrease in 3*/6 * Nicotinic Receptors but Not Nicotine- Evoked Dopamine Release in Monkey Brain after Nigrostriatal Damage

Nicotinic acetylcholine receptors (nAChRs) are decreased in the striata of patients with Parkinson’s disease (PD) or in ex-perimental models after nigrostriatal damage. Because presyn-aptic nAChRs on striatal dopamine terminals mediate dopa-mine release, receptor loss may contribute to behavioral deficits in PD. The present experiments were done to determine whether nAChR function is affected by nigrostriatal damage in nonhuman primates, because this model shares many features with PD. Initial characterization of nicotine-evoked [3H]dopa-mine release from monkey striatal synaptosomes revealed that release was calcium-dependent and inhibited by selective nAChR antagonists. It is noteworthy that a greater proportion (70%) of release was inhibited by the 3*/6 * antagonist -conotoxinMII (-CtxMII) compared with rodents. Monkey