Abstract
Focal application of 5 micrograms of morphine sulfate to the nucleus reticularis tegmenti pontis (NRTP) in rats reversed the akinesia induced by 5 mg/kg systemic haloperidol or 40 mg/kg systemic morphine and released festinating forward locomotion. gamma-Aminobutyric acid (200 micrograms) applied to this nucleus also reversed such akinesia. Intraventricular naloxone (10 micrograms) or picrotoxin (0.1 microgram), respectively, blocked the effects of such focally applied drugs. Thus, morphine and gamma-aminobutyric acid appear to act physiologically on the cells of the NRTP. The results suggest that systemic morphine, in addition to producing immobility, simultaneously facilitates a readiness for locomotion by inactivating a final common inhibitory system in the region of the NRTP.
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