Abstract
Intrathecal (i.t.) microinjection of 400 μg of morphine in rats induces convulsive activity restricted to the hindlimbs. This activity is potentiated rather than antagonized by naltrexone, is potentiated in animals pretreated over 6 days with increasingly higher systemic doses of morphine, and is potentiated and prolonged by high thoracic spinalization. Similar to morphine, convulsive spinal activity could also be elicited with i.t. injection of the non-opiate convulsant penthylenetetrazol (PTZ). However, methadone, d-ala 2-methionine-enkephalinamide (DALA), or naltrexone, injected i.t. at equimolar doses with morphine did not produce similar convulsive behavior. DALA and methadone rather produced pronounced spinal catalepsy. It was concluded: (1) that the spinal convulsive action of morphine is not mediated by specific opiate receptors; and (2) that the spinal cord may be one of the sites where high doses of systemically administered morphine may produce convulsions.
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