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- W2025746567 abstract "The acute administration of (+)-amphetamine sulphate to rats, induced a typical stimulant behavioural syndrome that was accompanied by depletion of cerebral glycogen and an elevation of lactate and malate. Pretreatment of rats with pimozide abolished the behavioural stimulation and the increase in malate but did not influence the fall in glycogen or increase in lactate induced by amphetamine. Conversely, prior administration of propranolol attenuated the amphetamine-induced changes in glycogen and lactate but neither prevented the hyperactivity nor the increase in cerebral malate. Cerebral injection of 6-hydroxydopamine, completely abolished the behavioural stimulation and cerebral metabolite changes induced by amphetamine. The administration of amphetamine to rats that had been chronically treated with the stimulant did not induce the characteristic rapid cerebral glycogenolysis but still caused behavioural stimulation and an elevation of cerebral malate. The involvement of catecholamines in cerebral glycogenolysis was emphasized by studies with L-DOPA which, in the presence of an extracerebral decarboxylase inhibitor, induced a profound and long-lasting depletion of the polysaccharide. In view of the dissociation of certain metabolic effects from behavioural stimulation, it is suggested that amphetamine may influence the release of dopamine which then acts at appropiate neuronal receptors, whereas released noradrenaline may interact with aβ-adrenoceptor on glia and there promote the breakdown of glycogen." @default.
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- W2025746567 date "1975-04-01" @default.
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- W2025746567 title "The role of catecholamines in the action of amphetamine and L-DOPA on cerebral energy metabolism" @default.
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- W2025746567 doi "https://doi.org/10.1016/0028-3908(75)90074-x" @default.
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