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Psychomotor stimulants increase regional cerebral metabolic rates for glucose (rCMRglc). To determine if effects in motor areas reflect limb movements, we measured rCMRglc in gallamine-paralyzed rats given cocaine, methylenedioxymethamphetamine, amphetamine, or phencyclidine. Results resembled findings in partially immobilized rats. One difference was lack of cocaine-induced stimulation in the caudate-putamen despite an increase in partially immobilized rats. Therefore, stimulant-induced rCMRglc stimulation in most motor areas is a primary CNS effect.

The 2-deoxy-D-[l-14C]glucose method was used to map the in vivo metabolic response (local cerebral glucose utilization. LCGU) to L-cocaine in the rat brain. Injections of L-cocaine HCl (30 mg/kg, i.p.) selectively enhanced LCGU in 5 out of 56 brain regions that were examined (caudate-putamen, globus pallidus, substantia nigra pars reticulata, subthalamic nucleus, cerebellar vermis), but 10 or 30 mg/kg L-cocaine reduced LCGU in the habenula. In general, the acute effects of L-cocaine on LCGU resembled previously reported effects of D-amphetamine and apomorphine.