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The serotonin "chemical imbalance" theory of depression, proposed in the 1960s, [35] is not supported by the available scientific evidence. [ 35 ] [ 36 ] SSRIs alter the balance of serotonin inside and outside of neurons: their clinical antidepressant effect (which is robust in severe depression [ 37 ] ) is likely due to more complex changes in ...
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]
One form of behavioral neuropharmacology focuses on the study of drug dependence and how drug addiction affects the human mind. Most research has shown that the major part of the brain that reinforces addiction through neurochemical reward is the nucleus accumbens. The image to the right shows how dopamine is projected into this area.
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.
Shortly after Schildkraut's catecholamine hypothesis was published, Coppen proposed that 5-HT, rather than NA, was the more important neurotransmitter in depression. This was based on similar evidence to that which produced the NA theory as reserpine, imipramine, and iproniazid affect the 5-HT system, in addition to the noradrenergic system.
The Monoamine Theory of Depression and Anxiety, which states that the disruption of the activity of nitrogen containing neurotransmitters (i.e. serotonin, norepinephrine, and dopamine) is strongly correlated with the presence of depressive symptoms. [9]
While depression is a complex condition with many factors involved, it is commonly attributed to an imbalance of several key monoamine neurotransmitters, including serotonin, dopamine and norepinephrine. This monoamine hypothesis of depression is popular because of the simplicity of the explanation. [4]
In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.
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