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BE AWARE that sertraline can potentially have drug interactions with a wide range of other medications, substances or supplements, like alcohol, monoamine oxidase inhibitors (MAOIs), nonsteroidal ...
Several meta-analytical studies have found increased levels of proinflammatory cytokines and chemokines in depressed patients. [190] This link has led scientists to investigate the effects of antidepressants on the immune system. SSRIs were originally invented with the goal of increasing levels of available serotonin in the extracellular spaces.
Sertraline, sold under the brand name Zoloft among others, is an antidepressant medication of the selective serotonin reuptake inhibitor (SSRI) class [10] used to treat major depressive disorder, generalized anxiety disorder, social anxiety disorder, obsessive–compulsive disorder (OCD), panic disorder, and premenstrual dysphoric disorder. [11]
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]
Common SSRIs include Prozac (fluoxetine), Zoloft (sertraline) and Lexapro (escitalopram). Effectiveness and side effect rates can vary between SSRIs. Effectiveness and side effect rates can vary ...
Additionally, some clinically used drugs such as chlorpheniramine, dextromethorphan, and methadone possess SRI properties secondarily to their primary mechanism of action(s) and this contributes to their side effect and drug interaction profiles. A closely related type of drug is a serotonin releasing agent (SRA), an example of which is ...
The decreased levels of NA proposed by Schildkraut, suggested that there would be a compensatory upregulation of β-adrenoceptors. Despite inconsistent findings supporting this, more consistent evidence demonstrates that chronic treatment with antidepressants and electroconvulsive therapy (ECT) decrease β-adrenoceptor density in the rat forebrain.
This interaction seems to be critical for increased availability of norepinephrine in or near the synaptic clefts. Actions of imipramine-like tricyclic antidepressants have complex, secondary adaptions to their initial and sustained actions as inhibitors of norepinephrine transport and variable blockade of serotonin transport.