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Increase of striatal Met5-enkephalin-Arg6-Phe7 (YGGFMRF) content elicited by long-term treatment with haloperidol.

In rats, daily doses of haloperidol repeated for various time periods increase striatal Met5-enkephalin-Arg6-Phe7 (YGGFMRF) immunoreactivity in a time- and dose-dependent manner. This increase occurred also in other dopamine-rich brain areas. After intraventricular captopril (0.5 mg), the accumulation rate of immunoreactive YGGFMRF was greater in haloperidol- than in saline-injected rats. Intraventricular captopril inhibits the YGGFMRF degradation; hence the greater accumulation rate of YGGFMRF caused by captopril in haloperidol-treated rats suggests that this drug increases the YGGFMRF biosynthesis. A slower rate of YGGFMRF release in haloperidol-treated rats can be excluded as a cause for the drug-induced increase in striatal content of this peptide because the release rates of YGGFMRF elicited by K+ were similar in striatal slices of haloperidol- and saline-treated rats. The similarities between the accumulation rate of immunoreactive YGGFMRF and of Met5-enkephalin induced by haloperidol suggest that haloperidol increases the biosynthesis of the specific messenger RNA for preproenkephalin, an opioid peptide precursor, which contains one copy of YGGFMRF and several copies of Met5-enkephalin.