Morphine's proconvulsant action: importance of endogenous norepinephrine.

The ability of morphine sulfate to lower the chemoconvulsant threshold was examined in mice pretreated with alpha-methyl-para-tyrosine (α-MT) methyl ester, FLA-63, phentolamine mesylate, L(-)-sotolol HCl, and pimozide. FLA-63, α-MT, and phentolamine pretreatment abolished the proconvulsant action of morphine, while L(-)-sotolol and pimozide pretreatment had no such effect. This suggests that endogenous norepinephrine (NE), but not endogenous dopamine (DA), is required for the expression of increased central excitability associated with the acute administration of morphine. Further, activation of central alpha-adrenergic receptors appears to be a requirement for morphine's proconvulsant action in the mouse.