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Abstract
In the rat, morphine and the opioid peptide [D-Ala2]-metenkephalinamide (D-ALA) increased the reaction time in the tail-flick test as well as the threshold for vocalization and vocalization afterdischarge after electrical stimulation of the tail. The analgesic effect of either opiate was potentiated by selective inhibition of brain type B MAO with deprenyl or pargyline and antagonized by selective inhibition of the A form of the enzyme with chlorgyline. β-Phenylethylamine (PEA), a specific substrate of brain type B MAO, also potentiated the opiate analgesia, and the enhancement was especially marked after combined treatments with deprenyl and PEA. The effect of PEA appeared to be preferentially related to the affective component of the pain response (threshold for vocalization afterdischarge). A more general role of PEA in brain function as a neuromodulator of the opiate receptor is proposed.
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