In rats treated with salmon calcitonin (CT) administered intracerebroventricularly (i.c.v., 85 or 8.5 pmol), spasmodic body movements, hopping and tail jerks, collectively termed dyskinesia, appeared within 1 h of administration and persisted for at least 24 h. In addition, spontaneous grooming, rearing and locomotion occurred less often in CT-treated rats than in vehicle-injected animals, while the incidence of both sniffing and nose poking remained essentially unchanged. The CT failed to displace either [3H]dopamine or [3H]spiperone from striatal membranes, and the behavioral effects were not blocked by haloperidol or SCH 23390, suggesting that the peptide did not directly affect dopamine receptors. The dyskinesia was not blocked by scopolamine, atropine, muscimol, diazepam or ketanserin. These data are consistent with the hypothesis that a compound with recognition characteristics similar to those of salmon CT may function as a neurotransmitter-modulator in the central nervous system.
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