THE ACTION OF DESMETHYLIMIPRAMINE IN COUNTERACTING SEDATION AND CHOLINERGIC EFFECTS OF RESERPINE-LIKE DRUGS

doi:10.1016/s0022-3565(25)26795-7

Paper

THE ACTION OF DESMETHYLIMIPRAMINE IN COUNTERACTING SEDATION AND CHOLINERGIC EFFECTS OF RESERPINE-LIKE DRUGS

Published Jun 1, 1964 · F. Sulser, M. Bickel, B. Brodie

The Journal of Pharmacology and Experimental Therapeutics

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133

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Abstract

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Study Snapshot

Desmethylimipramine (DMI) counteracts reserpine-like drug effects in rats by blocking cholinergic effects and sensitizing brain catecholamines to central adrenergic receptors.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

THE ACTION OF DESMETHYLIMIPRAMINE IN COUNTERACTING SEDATION AND CHOLINERGIC EFFECTS OF RESERPINE-LIKE DRUGS

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References

Citations

Animal models of depression in drug discovery: A historical perspective

Animal models of depression have been crucial in drug discovery, but their predictive validity needs further assessment.

Invited review: the evolution of antidepressant mechanisms

Monoamine antidepressants remain the best current medications for depression, but newer drugs with faster onsets and universal therapeutic action are being examined.

Role of norepinephrine in the pathophysiology and treatment of mood disorders

Norepinephrine plays a significant role in mood disorders, but its activity changes are less likely to be the primary cause of depression.

Acute and chronic effects of reserpine on biochemical and functional parameters of central and peripheral α2-adrenoceptors

Chronic treatment with reserpine increases the affinity of central and peripheral 2-adrenoceptors, resulting in biochemical and functional supersensitivity in the rat brain.

Chronic treatment with cholinesterase inhibitors increases α2-adrenoceptors in rat brain

Chronic treatment with cholinesterase inhibitors increases 2-adrenoceptors in rat brain, potentially contributing to mood alterations in individuals exposed to organophosphorus inhibitors.

Biochemical hypotheses on antidepressant drugs: a guide for clinicians or a toy for pharmacologists?

Antidepressants may not solely rely on blocking monoamine uptake, but rather involve changes in central monoamine transmission, with dopamine playing a key role in their clinical activity.

Rolipram, a novel antidepressant drug, reverses the hypothermia and hypokinesia of monoamine-depleted mice by an action beyond postsynaptic monoamine receptors

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Tetrabenazine-induced depletion of brain monoamines: characterization and interaction with selected antidepressants.

Tetrabenazine-induced depletion of brain monoamines can be counteracted by clorgyline and desmethylimipramine, with striatal DA and hypothalamic 5-HT being most sensitive to these effects.

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Electroconvulsive treatment and lithium carbonate both reduce norepinephrine metabolism in patients with primary, major depressions, highlighting a common effect of antidepressant treatments.