Nicotinic acetylcholine receptor (nAChR) activation is well known to stimulate dopamine release in the striatum. This phenomenon may be physiologically significant in the control of motor function, as well as in pathological conditions such as Parkinson's disease. An understanding of the mechanisms that influence nAChR expression and function is therefore important. Because the dopamine precursor L-DOPA is the most commonly used therapeutic agent for Parkinson's disease, we investigated the effects of L-DOPA treatment on striatal nAChR expression in unlesioned and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned monkeys. In unlesioned animals, L-DOPA (15 mg/kg) administered twice daily for 2 weeks decreased both 125 Parkinson's disease is a movement disorder characterized by a selective loss of nigrostriatal dopaminergic neurons, with marked declines in dopamine levels in the striatum. Knowledge of these neurochemical deficits led to the therapeutic use of the dopamine precursor L-DOPA, which is currently one of the principal agents used for Parkinson's disease therapy (Bezard et al., 2001).A variety of neurotransmitter systems regulate striatal dopaminergic function, including glutamatergic inputs from the cortex (Roberts and Anderson, 1979;Desce et al., 1991) and possibly serotonergic afferents from the raphe nuclei (Barnes and Sharp, 1999). Acetylcholine released from cholinergic interneurons is also an important modulating factor through activation of nAChRs (Zhou et al., 2001). Mammalian neuronal nAChRs are heterogeneous and seem to be composed of multiple ␣ (␣2-␣7) and  (2-4) subunits (Lukas et al., 1999). To date, several subtypes have been linked to striatal dopaminergic function, including nAChRs containing ␣4, ␣6, and 3 subunits in combination with 2 (Wonnacott, 1997; Quik et al., 2000;Grady et al., 2001;Champtiaux et al., 2002;Whiteaker et al., 2002;Zoli et al., 2002).Because nAChRs influence striatal dopaminergic activity, knowledge of the conditions that affect the different nAChR subtypes is critical. Studies to date have shown that nigrostriatal damage decreases striatal nAChR densities in mice, rats, monkeys, and humans, with a particular vulnerability of the 125 I-␣-CtxMII-binding population, thought to correspond to ␣6* 1 nAChRs (Schwartz et al., 1984;Clarke and Pert, 1985;Court et al., 2000;Quik et al., 2001;Zoli et al., 2002;Quik et al., 2003). Cholinergic pharmacological treat- 1 The asterisk denotes nicotinic receptors containing the indicated ␣ and/or  subunit and possibly also additional undefined subunits.