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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.
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 ...
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]
Symptoms must also cause clinically significant distress in important areas of everyday life (e.g. social or occupational). [22] For a diagnosis of a major depressive episode, the patient must also not have a history of manic or hypomanic episodes and their symptoms cannot meet the criteria for a mixed episode. [23]
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]
Other symptoms can include the inability to get excited about the pregnancy, and/or baby, a feeling of disconnection with the baby, and an inability to form/feel a bond with the developing baby. [7] This can drastically affect the relationship between the mother and the baby, and can drastically affect the mother's capacity for self-care.
A meta-analysis found that up to 12.7% of pregnant women experience an episode of major depression, while as many as 18.4% experience depression at some point in their pregnancy. [4] However, they did not find a significant difference between these and rates of depression in women at nonchildbearing times.
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