Evidence for the involvement of central opioidergic systems in L-tyrosine methyl ester-induced analgesia in the rat.

Abstract

Intraperitoneal administration of L-tyrosine (used as methyl ester HCl) produced dose-dependent analgesia in male Sprague-Dawley rats as measured by the tail-flick test. The maximal analgesic response was obtained with 200 mg/kg dose of tyrosine. Administration of morphine also produced a dose-dependent analgesic response. Tyrosine in doses of 50 mg/kg or higher potentiated morphine-induced analgesia. The analgesic response of tyrosine (200 mg/kg) was antagonized by naloxone (1 mg/kg), an opiate antagonist. Subcutaneous administration of methyl naltrexone bromide (MRZ 2663 BR, 1 and 10 mg/kg) had no effect on tyrosine-induced analgesia. Intracerebroventricular injection of MRZ 2663 BR (1 and 10 micrograms/rat) effectively blocked tyrosine-induced analgesia. It is concluded that tyrosine-induced analgesia and its potentiation of analgesic response to morphine may be mediated via either the opiate receptors or activation of endogenous opioidergic systems of central origin.