Abstract
The neuropharmacologic mechanisms underlying neuroleptic-induced extrapyramidal syndromes (EPS) were studied using a nonhuman primate model. Twenty-six Cebus albifrons monkeys were given weekly challenges of haloperidol (0.025 mg/kg IM), and half of the animals received the monoamine oxidase (MAO) inhibitor pargyline (5 mg/kg PO) daily for 17 consecutive days during the protocol. Pargyline caused no changes in baseline behaviors, but significantly reduced haloperidol-induced acute dystonia (AD) (-67%, P<0.002) and parkinsonism (-56%, P<0.005). The majority (8 of 13) of the experimental group had complete prevention of neuroleptic-induced EPS during cotreatment with pargyline. Behavioral scores returned to baseline levels after stopping pargyline, and did not show the further sensitization to haloperidol-induced AD that occurred in the control group. The possible mechanisms by which an MAO inhibitor might influence neuroleptic-induced AD were considered. The most likely explanation would appear to involve facilitation of striatal dopamine (DA) neurotransmission by inhibition of intra- and extraneuronal MAO, thus supporting the hypothesis that AD is due to decreased striatal DA function with secondary cholinergic hyperfunction.
Original language | English (US) |
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Pages (from-to) | 207-213 |
Number of pages | 7 |
Journal | Psychopharmacology |
Volume | 93 |
Issue number | 2 |
DOIs | |
State | Published - Oct 1987 |
Keywords
- Cebus albifrons monkeys
- Dystonia
- Extrapyramidal syndromes
- Monoamine oxidase
- Neuroleptics
- Pargyline
- Primates
ASJC Scopus subject areas
- Pharmacology