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Trazodone, sold under many brand names, [1] is an antidepressant medication [20] used to treat major depressive disorder, anxiety disorders, and insomnia. [20] It is a phenylpiperazine compound of the serotonin antagonist and reuptake inhibitor (SARI) class.
These drugs act as antagonists or inverse agonists of the 5-HT 2A, α 1-adrenergic, and H 1 receptors, as partial agonists of the 5-HT 1A receptor, [3] and as inhibitors of the transporters. mCPP is an antagonist of the 5-HT 2B receptor, an agonist of the 5-HT 1A, [3] 5-HT 2C, and 5-HT 3 receptors, [4] [5] and acts as a partial agonist of the ...
In addition to their actions as reuptake inhibitors of serotonin, some SSRIs are also, coincidentally, ligands of the sigma receptors. [ 187 ] [ 188 ] Fluvoxamine is an agonist of the σ 1 receptor , while sertraline is an antagonist of the σ 1 receptor, and paroxetine does not significantly interact with the σ 1 receptor.
Rare (<0.1%) adverse effects include: Urinary retention; Prolonged QT interval; Torsades de Pointes; Ataxia; Breast enlargement or engorgement; Lactation; Cardiospasm
This is a complete list of clinically approved prescription antidepressants throughout the world, as well as clinically approved prescription drugs used to augment antidepressants or mood stabilizers, by pharmacological and/or structural classification.
An atypical antidepressant is any antidepressant medication that acts in a manner that is different from that of most other antidepressants. Atypical antidepressants include agomelatine, bupropion, iprindole, mianserin, mirtazapine, nefazodone, opipramol, tianeptine, and trazodone.
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]
The pharmacology of antidepressants is not entirely clear.. The earliest and probably most widely accepted scientific theory of antidepressant action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the monoamine neurotransmitters (namely serotonin, norepinephrine and dopamine). [1]