[On the proposed mechanism of action of antidepressants (author's transl)].
Classical antidepressants (MAOI, uptake inhibitors) increase monoamine levels in the synaptic cleft. However other presynaptic mechanisms of action have been proposed: increase in release (amineptin), blockade of presynaptic alpha-adrenoceptors (mianserin). A postsynaptic approach is also possible: stimulation of beta-receptor (salbutamol), blockade of muscarinic receptor (quinupramine). Moreover the side effects have been correlated to a blockade of postsynaptic receptors: alpha 1 for aorthostatic hypotension, H1 for sedation and muscarinic for anticholinergic effects. However these effects do not explain the delay for the clinical efficiency of antidepressants. A desensitization of presynaptic receptors or a decrease in beta-postsynaptic receptors have been advanced. In fact a possible pharmacokinetic explanation for the delay of clinical efficiency, i.e. the necessary delay to reach brain steady state level, is possible. Finally the presence of imipramine binding sites might be a new approach of the mechanism of action of antidepressants.
D000818:Animals; D000928:Antidepressive Agents / Q000009:adverse effects / Q000494:pharmacology*; D001665:Binding Sites; D001679:Biogenic Amines / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D007099:Imipramine / Q000378:metabolism; D007700:Kinetics; D051379:Mice; D008996:Monoamine Oxidase Inhibitors; D051381:Rats; D017981:Receptors, Neurotransmitter / Q000187:drug effects; D013997:Time Factors
D000928:Antidepressive Agents; D001679:Biogenic Amines; D008996:Monoamine Oxidase Inhibitors; D017981:Receptors, Neurotransmitter; D007099:Imipramine
A propos du mécanisme d'action supposé des antidépresseurs.