A new animal model for action myoclonus.

E. Shohami, S. Evron, M. Weinstock, D. Soffer, A. Carmon

Research output: Contribution to journalArticlepeer-review

Abstract

Morphine was injected into a catheter implanted chronically into the intrathecal space of rats. Three to eight minutes after drug administration, 80% of the rats developed arrhythmic stimulus-sensitive jerks that lasted up to 1 hr. The morphine-induced myoclonic activity was markedly reduced by naloxone. Methadone, pethidine, and etorphine failed to produce the syndrome. In spinally transected rats, morphine injected below the level of transection did not produce the syndrome. No significant changes in PaCO2 and PaO2 were produced by morphine before and throughout the period of myoclonic activity. Neither did induced hypoxia augment the effect of morphine. However, irreversible hypoxic-ischemic cell changes were noticed in some brain regions. The phenomenon described here resembles the human syndrome of action myoclonus and may serve as an animal model for studying the mechanism of that neurological disorder.

Original languageEnglish
Pages (from-to)545-552
Number of pages8
JournalAdvances in neurology
Volume43
StatePublished - 1986

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