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Abstract

Specific effects of opiate narcotics on rat flexor agr-motoneurones were studied in ventral roots of laminectomized rats under halothane anaesthesia. The agr-motoneurones were activated by tetanic stimulation of the cut ipsilateral common peroneal nerve, exciting up to group II- but not group III- and C-afferents. Morphine (0.5–3.0 mg/kg i.v.) reduced or completely suppressed the discharge rate of flexor agr-motoneurones in a dose-dependent manner. This effect was antagonized by naloxone (0.5 mg/kg i.v.) and mimicked by levorphanol (1.0 mg/kg i.v.), but not by an equal dose of its steroisomer dextrorphan, suggesting that the effect described is a specific one. After spinalization, the inhibitory effect of morphine was abolished. Previous studies had shown that opiates (e.g. morphine, given in a dose of 2 or 4 mg/kg i.v.) excite rat extensor agr-motoneurones, an effect opposite to the opiate narcotic action on flexor agr-motoneurones. The action of opiates leading to an inhibition of flexor agr-motoneurones may contribute to akinesia and catalepsy, and opioid-induced muscular rigidity. From the results presented it appears that morphine produces a reciprocal change in the activity evoked in extensor and flexor reflex pathways.

Key words  Motoneurones - Flexor agr-motoneurones - Opiate narcotics - Morphine - Naloxone

Some of these results were presented at the 18th Spring Meeting of the German Pharmacological Society, Mainz, March 16–18, 1977
These studies were supported by a grant (B-3) from the Sonder-forschungsbereich 33 ldquoNervensystem und biologische Informationrdquo of the Deutsche Forschungsgemeinschaft

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