Behavioral recovery from MPTP-induced parkinsonism in monkeys after intracerebral tissue implants is not related to CSF concentrations of dopamine metabolites

l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP) administered to primates causes the rapid development of a movement disorder that closely resembles Parkinson's disease. The toxicity of MPTP depends on its conversion by monoamine oxidase B to its pyridinium derivative, MPP +, which is concentrated selectively in catecholaminergic neurons. Data presented in the chapter are the part of a multidisciplinary study of MFTP effects and the ability of implanted tissue grafts to reverse the MPTP-induced motor deficits in nonhuman primates. The survival of fetal mesencephlic tissue implanted into the primate neostriatum and at least a partial reversal of the MPTP-induced motor deficits has been demonstrated in monkeys. Surviving implanted dopaminergic neurons can synthesize, store, and release dopamine; they also can form processes that are believed to innervate the damaged host neostriatum. The implantation of nondopaminergic fetal amniotic tissue also elicits behavioral recovery. The behavioral recovery in MPTP-hemiparkinsonian monkeys after fetal dopaminergic implants is a consequence of stimulation of growth of host dopaminergic neuronal sprouts rather than the result of secretion of dopamine by the graft or ingrowth of fibers from the dopamine-rich implant. The chapter examines whether biochemical alterations in the cerebrospinal fluid (CSF) reflect the apparent changes in dopaminergic function, which attend the development of hemiparkinsonism in rhesus monkeys after a unilateral intracarotid artery infusion of MPTP and after the implantation of various tissue grafts that produce transient or permanent functional motor improvement in these animals.