The inhibition of movement by morphine or haloperidol depends on an intact nucleus reticularis tegmenti pontis

Rebecca M. Chesire, Jung Tung Cheng, Philip Teitelbaum

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

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 μg γ-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.

Original languageEnglish (US)
Pages (from-to)809-818
Number of pages10
JournalPhysiology and Behavior
Volume30
Issue number5
DOIs
Publication statusPublished - May 1983
Externally publishedYes

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Keywords

  • Akinesia
  • Festination
  • GABA
  • Haloperidol
  • Morphine
  • Movement subsystems
  • Nucleus reticularis tegmenti pontis
  • Parkinson's disease

ASJC Scopus subject areas

  • Experimental and Cognitive Psychology
  • Behavioral Neuroscience

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