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G Wilkerson

Publications and source records attributed to G Wilkerson.

6 recordsLinked to original sources

Central action of psychomotor stimulants on glucose utilization in extrapyramidal motor areas of the rat brain.

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.

3,4-Methylenedioxyamphetamine↗

Effects of methylenedioxymethamphetamine on local cerebral glucose utilization in the rat.

The effects of (+-)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") (5, 10, 15 or 30 mg/kg, i.p.) on local cerebral utilization of glucose were studied by the quantitative autoradiographic 2-deoxy-D-[1-14C]glucose method in awake adult male Fischer-344 rats. Statistically significant effects on local utilization of glucose, 5 min after the administration of MDMA were observed in 20 of 60 areas of brain sampled. Marked stimulation was seen in components of the extrapyramidal motor system (substantia nigra, globus pallidus, entopenduncular nucleus, subthalamic nucleus, cerebellar vermis). The limbic system showed decrements in the medial cortex and hippocampal dentate gyrus (outer blade) and the lateral habenula, while there was stimulation in the mammillary body and the basolateral amygdaloid nucleus. Glucose utilization in MDMA-treated rats was reduced in the superior colliculus and medial terminal nucleus of the accessory optic system, but was unchanged in the visual cortex and components of the auditory system. Some of the effects of MDMA on cerebral utilization of glucose resembled those previously reported with l-cocaine, d-amphetamine, and phencyclidine, implicating some common mechanisms in the actions of these drugs.

3,4-Methylenedioxyamphetamine↗

Effects of L-cocaine on local cerebral glucose utilization in the rat.

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.

Animals↗