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The major limitation of SSRIs concerns their delay of action. It appears that the clinical efficacy of SSRIs becomes evident only after a few weeks. [225] SSRIs can be combined with a host of other drugs including bupropion, α 2 adrenergic antagonists (e.g., yohimbine) as well as some of the atypical antipsychotics. The augmentation agents are ...
The following antidepressants are available both with a prescription and over-the-counter: Ademetionine [S-Adenosyl-L-methionine (SAMe)] (Heptral, Transmetil, Samyl) – cofactor in monoamine neurotransmitter biosynthesis; Hypericum perforatum [St. John's Wort (SJW)] (Jarsin, Kira, Movina) – TRPC6 activator, and various other actions
Use of antidepressants during pregnancy may result in fetus abnormalities affecting functional development of the brain and behavior. [90] Studies have shown correlations between pregnant women treated with SNRIs and risk of hypertensive disorders, [91] preeclampsia, [92] miscarriage, [93] seizures in children, [94] and many other adverse affects.
SSRIs (selective serotonin reuptake inhibitors), which debuted in the 1980s, work on serotonin. SNRIs (serotonin and norepinephrine reuptake inhibitors) hit serotonin and norepinephrine.
Fluoxetine, sold under the brand name Prozac, among others, is an antidepressant medication of the selective serotonin reuptake inhibitor (SSRI) class [2] used for the treatment of major depressive disorder, anxiety, obsessive–compulsive disorder (OCD), panic disorder, premenstrual dysphoric disorder, and bulimia nervosa. [2]
A GABA reuptake inhibitor (GRI) is a type of drug which acts as a reuptake inhibitor for the neurotransmitter gamma-Aminobutyric acid (GABA) by blocking the action of the gamma-Aminobutyric acid transporters (GATs). This in turn leads to increased extracellular concentrations of GABA and therefore an increase in GABAergic neurotransmission. [1]
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]
Cross-tolerance is a phenomenon that occurs when tolerance to the effects of a certain drug produces tolerance to another drug. It often happens between two drugs with similar functions or effects—for example, acting on the same cell receptor or affecting the transmission of certain neurotransmitters.