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Effect of depletion of cerebral monoamines on the concentration of glycogen and on amphetamine‐induced glycogenolysis in the brain
Author(s) -
HUTCHINS D. A.,
ROGERS K. J.
Publication year - 1973
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1973.tb08218.x
Subject(s) - reserpine , glycogenolysis , amphetamine , chemistry , endocrinology , monoamine neurotransmitter , medicine , catecholamine , glycogen , cerebral cortex , adrenergic , pharmacology , dopamine , receptor , serotonin , biochemistry , biology
Summary1 An increase in the concentration of glycogen occurs in the mouse brain after depletion of cerebral catecholamines by alpha methyl‐ p ‐tyrosine methylester (H44/68), diethyldithiocarbamate, or reserpine. 2 Depletion of cerebral 5‐hydroxytryptamine with parachlorophenylalanine (PCPA) does not result in a change in the concentration of brain glycogen. 3 When H44/68 is administered together with reserpine to inhibit the synthesis and storage of cerebral catecholamines, and thus bring about their total depletion from the brain, the cerebral glycogenolytic effect of amphetamine is abolished. 4 Amphetamine‐inducing glycogenolysis is only partially antagonized if only one of the catecholamine‐depleting agents H44/68, diethyldithiocarbamate, or reserpine is injected prior to the amphetamine. The persistence of this glycogenolytic effect of amphetamine is possibly due to the presence of residual stores of catecholamines available for release by the stimulant drug. 5 Depletion of cerebral 5‐hydroxytryptamine by PCPA does not result in any antagonism of amphetamine‐induced glycogenolysis. 6 The results suggest that amphetamine depletes brain glycogen by the release of central catecholamines rather than by a direct action at receptors.