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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.
Niaprazine (Nopron) – a drug related to this group but does not inhibit the reuptake of serotonin or the other monoamines. Medifoxamine (Clédial, Gerdaxyl) – could perhaps technically be said to belong to this group, as it is a serotonin–dopamine reuptake inhibitor and 5-HT 2A and 5-HT 2C receptor antagonist, but not grouped as such. [1]
This is a list of adverse effects of the antidepressant trazodone, sorted by frequency of occurrence. [1] [2] [3] Very common.
Concomitant use of SSRIs or SNRIs for depression with a triptan for migraine does not appear to heighten the risk of the serotonin syndrome. [120] Taking monoamine oxidase inhibitors (MAOIs) in combination with SSRIs can be fatal, since MAOIs disrupt monoamine oxidase , an enzyme which is needed to break down serotonin and other neurotransmitters.
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.
Studies have found that magnesium or trazodone can help treat the persisting withdrawal symptom of insomnia in recovering alcoholics. Insomnia can be difficult to treat in these individuals because many of the traditional sleep aids (e.g., benzodiazepine receptor agonists and barbiturate receptor agonists) work via a GABA A receptor mechanism ...
With the exception of amoxapine, TeCAs do not inhibit the reuptake of serotonin [citation needed]. However, aside from mirtazapine, they do inhibit the reuptake of norepinephrine [citation needed]. TeCAs block the serotonin 5-HT 2 receptors similarly to TCAs. Besides mirtazapine, they also block the α 1-adrenergic receptor [citation needed].
It does not bind to blood cells. [2] The drug is known to cross the placental barrier. [2] Etifoxine is metabolized in the liver into several metabolites. [5] One of these metabolites, diethyletifoxine, is pharmacologically active. [5] The elimination half-life of etifoxine is 6 hours and of diethyletifoxine is almost 20 hours. [5]
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