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Mirtazapine is a very strong H 1 receptor antagonist and, as a result, it can cause powerful sedative and hypnotic effects. [11] A single 15 mg dose of mirtazapine to healthy volunteers has been found to result in over 80% occupancy of the H 1 receptor and to induce intense sleepiness . [ 92 ]
A number of non-SSRI drugs are not associated with sexual side effects (such as bupropion, mirtazapine, tianeptine, agomelatine, tranylcypromine, and moclobemide [57] [58] [59]). Several studies have suggested that SSRIs may adversely affect semen quality. [60] [61]
[38] [39] The condition has however occurred in surprising clinical situations, and because of phenotypic variations among individuals, it has been associated with unexpected drugs, including mirtazapine. [40] [41] The relative risk and severity of serotonergic side effects and serotonin toxicity, with individual drugs and combinations, is complex.
Because of its lack of anticholinergic side effects, trazodone is especially useful in situations in which antimuscarinic effects are particularly problematic (e.g., in patients with benign prostatic hyperplasia, closed-angle glaucoma, or severe constipation). Trazodone's propensity to cause sedation is a dual-edged sword.
In addition, due to their blockade of certain serotonin receptors, serotonergic neurotransmission is not facilitated in unwanted areas, which prevents the incidence of many side effects often associated with selective serotonin reuptake inhibitor (SSRI) antidepressants; [1] [3] hence, in part, the "specific serotonergic" label of NaSSAs. [2]
[8] [1] Unlike low-dose mirtazapine, the half life (10 hours) is short enough that next-day sedation may be manageable, however, for people with CYP2D6 polymorphisms, which constitute a sizable fraction of the population, the half-life is expected to be quite a bit longer. Merck researchers claimed that the incidence of next-day sedation was ...
The tetracyclic antidepressants mianserin and mirtazapine are α 2 blockers, although their efficacy as antidepressants may come from their activity at other receptor sites. [citation needed] Mechanistically, α 2 blockers increase adrenergic, dopaminergic and serotonergic neurotransmitters and induce insulin secretion, decreasing blood sugar ...
Besides mirtazapine, they also block the α 1-adrenergic receptor [citation needed]. Conversely, whereas TCAs have relatively low affinity for the α 2 -adrenergic receptor , mianserin and mirtazapine potently antagonize this receptor, and this action is thought to be involved in their antidepressant effects [ citation needed ] .
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