Abstract
The β-endorphin (βE) fragment des-Tyr 1-γ-endorphin (DTγE, βE-(2–17)) has been reported to interact with neuroleptic binding in vivo but not in vitro. We have attempted to replicate the in vivo experiments and extended the work to include conditions in which des-enkephalin-γ-endorphin (DEγE, βE-(6–17)) exhibited behavioral activity. Systematically administered haloperidol significantly elevated plasma and decreased striatal [ 3H]spiperone. DEγE significantly elevated plasma [ 3H]apomorphine when both substances were injected directly into the nucleus accumbens. γ-type endorphins consistently but non significantly decreased brain spiperone or apomorphine binding. It is concluded that the interaction between γ-type endorphins and dopaminergic binding sites may be either indirect or limited to a subset of these sites.
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