Abstract
Lateral intraventricular (LV) or cerebral aqueduct (CA) administration of the opioid peptide, dynorphin-(1-13), induced catalepsy and analgesia in rats. Onset was earlier and duration shorter than with morphine or β c-endorphin. The dose required to induce analgesia was reduced at least tenfold when dynorphin-(1-13) was administered into CA rather than LV. An analogue, D-Ala 2-dynorphin-(1-11), was more stable than dynorphin-(1-13) in brain, and produced a comparable degree of catalepsy and even more profound analgesia at one-tenth the dose. These effects of dynorphin-(1-13) and D-Ala 2-dynorphin-(1-11) were significantly antagonized by naloxone pretreatment. Rats treated with dynorphin-(1-13) or a high dose of D-Ala 2-dynorphin-(1-11) exhibited bizarre postures immediately following LV administration, with limb rigidity and “barrel-rolling”. These effects were not blocked by naloxone.
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