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The main limitation for the monoamine hypothesis of depression is the therapeutic lag between initiation of antidepressant treatment and perceived improvement of symptoms. One explanation for this therapeutic lag is that the initial increase in synaptic serotonin is only temporary, as firing of serotonergic neurons in the dorsal raphe adapt via ...
The neurotrophic hypothesis of depression [1] proposes that major depressive disorder (MDD) is caused, at least partly, by impaired neurotrophic support.Neurotrophic factors (also known as neurotrophins) are a family of closely related proteins which regulate the survival, development, and function of neurons in both the central and peripheral nervous systems.
However, the hypothesis is incomplete, as several lines of evidence suggests that depression is more than just a monoamine imbalance. For example, antidepressants usually take several weeks to reduce a patient's depressive symptoms, which is inconsistent with the finding that monoamine levels are affected within hours of using antidepressants. [5]
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.
After release into the synaptic cleft, monoamine neurotransmitter action is ended by reuptake into the presynaptic terminal. There, they can be repackaged into synaptic vesicles or degraded by the enzyme monoamine oxidase (MAO), which is a target of monoamine oxidase inhibitors, a class of antidepressants. [citation needed]
The two main symptoms of a major depressive episode are a depressed mood and a loss of interest or pleasure. [3] From the list below, one bold symptom and four other symptoms must be presented for at least 2 weeks for a diagnosis of a major depressive episode. Weight loss or gain; Change in body activity (psychomotor changes) Change in sleep ...
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]
Based on the monoamine hypothesis of depression, which asserts that decreased concentrations of monoamine neurotransmitters leads to depressive symptoms, the following relations were determined: "Norepinephrine may be related to alertness and energy as well as anxiety, attention, and interest in life; [lack of] serotonin to anxiety, obsessions ...
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