Opiates Stimulate Low Km GTPase in Brain

Abstract
Low Km GTp hydrolysis in rat brain is stimulated in a concentration-dependent manner by the opiate alkaloid etorphine, and by the opioid peptide D-Ala2-leucine-enkephalinamide. The opiate antagonist naloxone inhibits the maximal D-Ala2-leucine-enkephalinamide stimulation of the GTPase, also with concentration dependency. The magnitude of maximally stimulated, opioid-sensitive, GTP hydrolysis is differentially distributed across brain regions. Opioid-stimulated GTPase may represent 1 means of identifying a specific type of opioid receptor.