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 language | English (US) |
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Pages (from-to) | 809-818 |
Number of pages | 10 |
Journal | Physiology and Behavior |
Volume | 30 |
Issue number | 5 |
DOIs | |
State | Published - May 1983 |
Externally published | Yes |
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