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5-HTTLPR (serotonin-transporter-linked promoter region) is a degenerate repeat (redundancy in the genetic code) polymorphic region in SLC6A4, the gene that codes for the serotonin transporter. Since the polymorphism was identified in the middle of the 1990s, [ 1 ] [ 2 ] it has been extensively investigated, e.g., in connection with ...
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 ...
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.
They act by antagonizing the α 2-adrenergic receptor and certain serotonin receptors such as 5-HT 2A and 5-HT 2C, [1] but also 5-HT 3, [1] 5-HT 6, and/or 5-HT 7 in some cases. By blocking α 2 -adrenergic autoreceptors and heteroreceptors , NaSSAs enhance adrenergic and serotonergic neurotransmission in the brain involved in mood regulation ...
BDNF is involved in depression through its effects on serotonin. BDNF has been shown to promote the development, function, and expression of serotonergic neurons. [28] Because more active serotonin results in more positive moods, antidepressants work to increase serotonin levels.
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]
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