The inhibition of movement by morphine or haloperidol depends on an intact nucleus reticularis tegmenti pontis.
Electrolytic damage of the nucleus reticularis tegmenti pontis (NRTP) in rats produces a form of accelerating forward locomotion, indicating that this region is part of a system that inhibits locomotion and movement. In animals with such damage, 5 mg/kg haloperidol does not block forward locomotion although it produces complete akinesia in normal rats [2]. Our present results demonstrate that doses of morphine sulfate that render normal rats completely akinetic (40, 50, or 60 mg/kg) also fail to block forward locomotion. Furthermore, 200 micrograms gamma-aminobutyric acid applied intracranially in the region of the NRTP can reverse the akinesia produced by systemically administered haloperidol or morphine. We suggest that there are two types of akinesia--direct and indirect--and that morphine and haloperidol may produce akinesia indirectly via an inhibitory system which includes the NRTP.
D000818:Animals; D006220:Haloperidol / Q000494:pharmacology*; D008297:Male; D009020:Morphine / Q000494:pharmacology*; D009043:Motor Activity / Q000187:drug effects*; D009048:Motor Skills / Q000187:drug effects; D009115:Muridae; D011149:Pons / Q000187:drug effects*; D051381:Rats; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D005680:gamma-Aminobutyric Acid; D009020:Morphine; D006220:Haloperidol