Abstract
Morphine (1.0 mg/kg), ACTH 1–24 (10.0 μg/kg), epinephrine (12.0 μg/kg), Met-enkephalin (2.0 and 5.0 μg/kg), Leu-enkephalin (2.0 μg/kg) and des-Tyr-Met-enkephalin (2.0 μg/kg) all produced marked reductions of β-endorphin-like immunoreactivity in the rat diencephalon. At a dose of 0.4 mg/kg, naloxone had no effect of its own and was unable to reverse the depleting effect of the other substances. The depletion of β-endorphin-like immunoreactivity caused by the various treatments is attributable to release and subsequent degradation of β-endorphin and/or of its precursors. The various behavioral effects of morphine, ACTH, epinephrine and the enkephalins may be explained by the release of endogenous β-endorphin.
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