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First, serotonin system dysfunction cannot be the sole cause of depression, because not all patients treated with antidepressants show improvement, despite the fact that most patients still show a rapid increase in synaptic serotonin. Second, if significant mood improvements do occur, this is often not for at least two to four weeks.
Serotonin's association with mood is most known for various forms of depression and bipolar disorders in humans. [201] Disorders caused by serotonergic activity potentially contribute to the many symptoms of major depression, such as overall mood, activity, suicidal thoughts and sexual and cognitive dysfunction.
This article needs to be updated. The reason given is: Many outdated sources and information (older than five years). Please help update this article to reflect recent events or newly available information. (July 2024) Medical condition Major depressive disorder Other names Clinical depression, major depression, unipolar depression, unipolar disorder, recurrent depression Specialty Psychiatry ...
It is difficult to develop an animal model that perfectly reproduces the symptoms of depression in patients. It is generic that 3 standards may be used to evaluate the reliability of an animal version of depression: the phenomenological or morphological appearances (face validity), a comparable etiology (assemble validity), and healing similarities (predictive validity).
[12] [13] [14] One interpretation is that depression manifests due to an imbalance of neurotransmitters in the brain, resulting in feelings of worthlessness and despair. Magnetic resonance imaging shows that the brains of people diagnosed with depression may have a hippocampus up to 10% smaller than those who do not exhibit signs of depression.
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The serotonin transporter (SERT or 5-HTT) also known as the sodium-dependent serotonin transporter and solute carrier family 6 member 4 is a protein that in humans is encoded by the SLC6A4 gene. [5] SERT is a type of monoamine transporter protein that transports the neurotransmitter serotonin from the synaptic cleft back to the presynaptic ...
Serotonin pathways are thought to modulate eating, both the amount as well as the motor processes associated with eating. The serotonergic projections into the hypothalamus are thought to be particularly relevant, and an increase in serotonergic signaling is thought to generally decrease food consumption (evidenced by fenfluramine , however ...