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Blockade of cholecystokinin-A receptors has no effect on dyskinesias in Parkinson's disease

Cholecystokinin is one of the most abundant neuropeptides in the human CNS. It coexists with dopamine in ventral tegmental and substantia nigra neurons in rodents and primates, but the coexistence is less obvious in normal humans.1 It modulates central motor effects of dopamine through nigral or striatal cholecystokinin-A (excitatory) and cholecystokinin-B (inhibitory) receptors. The effect of the neuropeptide differs, however, depending on the animal species, the dose used, cotreatments, and site of injection.

Cholecystokinin is selectively decreased in the substantia nigra of patients with Parkinson's disease, and cholecystokinin-A antagonist binding is reduced in hemiparkinsonian monkeys. Cholecystokinin inhibits levodopa induced dyskinesias in parkinsonian monkeys,1 but proglumide, a cholecystokinin antagonist, did not improve motor signs in dyskinesia free patients with Parkinson's disease.2 Proglumide is, however, a weak non-selective cholecystokinin antagonist. Oral SR 27897B (SR; Sanofi Recherche), a highly selective and potent cholecystokinin-A receptor antagonist, penetrates the CNS and blocks cholecystokinin potentiation of dopaminergic neurotransmission.3 We evaluated the potential antidyskinetic effects of oral SR in parkinsonian patients using a placebo controlled double blind study design and a single challenge of apomorphine, a test used to determine the antidyskinetic properties of associated treatments.4 As cholecystokinin-A antagonism may modify gastrointestinal motility,3 and consequently the kinetics of oral …