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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 ...
A 2003 study proposed that a gene-environment interaction (GxE) may explain why life stress is a predictor for depressive episodes in some individuals, but not in others, depending on an allelic variation of the serotonin-transporter-linked promoter region . [15]
HDAC inhibitors can decrease gene transcription in the hippocampus and prefrontal cortex that is increased as a characteristic of depression. In animal studies of depression, short-term administration of HDAC inhibitors reduced the fear response in mice, and chronic administration produced antidepressant-like effects.
Tametraline, a compound synthesized in 1978 by Pfizer, was shown to be a potent NE and DA re-uptake inhibitor with animal studies. [6] Later on a surprisingly substantial enhancement of blocking activity of 5-HT uptake was achieved by adding chlorine atoms at C-3 and C-4 to the structure of tametraline, resulting in (+)- trans -(1 R ,4 S )- N ...
Data also shows that using pro-inflammatory agents in the treatment of diseases like melanoma can lead to depression. 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.
The 7 general serotonin receptor classes include a total of 14 known serotonin receptors. [9] The 15th receptor 5-HT 1P has been distinguished on the basis of functional and radioligand binding studies, its existence has never been definitely affirmed or refuted. [10] [11] The specific types have been characterized as follows: [12] [13] [14]
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]
Recent studies have shown that depression may be linked to increased inflammatory response, [54] thus attempts at finding an additional mechanism for SNRIs have been made. Studies have shown that SNRIs as well as SSRIs have significant anti-inflammatory action on microglia [55] in addition to their effect on serotonin and norepinephrine levels ...