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THE EFFECT OF PARGYLINE AND DESMETHYLIMIPRAMINE ON MONOAMINE CONCENTRATIONS AND AMPHETAMINE‐INDUCED GLYCOGENOLYSIS IN THE MOUSE BRAIN
Author(s) -
HUTCHINS D.A.
Publication year - 1979
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.1476-5381.1979.tb07856.x
Subject(s) - pargyline , amphetamine , endocrinology , desipramine , medicine , monoamine neurotransmitter , chemistry , monoamine oxidase , glycogenolysis , neuroscience , serotonin , dopamine , biology , metabolism , biochemistry , antidepressant , enzyme , receptor , hippocampus
1 Pargyline (100 mg/kg) increased the concentration of cerebral noradrenaline dopamine and 5‐hydroxytryptamine in the mouse. Amphetamine (5 mg/kg) reduced the concentration of noradrenaline and increased the concentrations of 5‐hydroxytryptamine and dopamine. 2 When amphetamine was administered 4 h after an injection of pargyline, the effect of the sympathomimetic drug on the concentrations of noradrenaline and 5‐hydroxytryptamine was not altered. The effect on the dopamine content was reversed, amphetamine causing a decrease instead of an increase. 3 Pargyline increased the concentration of cerebral glycogen, whereas amphetamine caused a decrease. 4 The administration of amphetamine 4 h after pargyline resulted in a decrease in brain glycogen similar to that seen after amphetamine alone. 5 These results suggest that the potentiation of the effect of amphetamine on animal behaviour by pretreatment with an inhibitor of monoamine oxidase is not mediated through a central action on noradrenaline release. 6 Amphetamine‐induced glycogenosis was antagonized by 71% by desmethylimipramine (10 mg/kg). 7 The change in glycogen concentration as a function of time after an injection of amphetamine was not modified when 2 consecutive doses of amphetamine were given with an interval between doses of 30 minutes.