Intrathecal substance P analogue causes motor dysfunction in the rat.

(D-Pro2, Trp7,9)-substance P injected into the subarachnoid space produced a severe faccid extension of hindlimb in a dose-related manner in the rat. This motor dysfunction was neither reversed by naloxone, an opioid receptor antagonist nor by intrathecal SP. SP levels in the lumbar cord were markedly depleted in rats with hindlimb paralysis, though there was not significant changes in rats without paraplegia. These results suggest that DPDT-SP produces motor dysfunction which dose not appear to be mediated by opioid and SP receptors.