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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 ...
The bound receptor is involved in the regulation of gene transcription. [4] [24] The GR gene promoter region has a sequence that allows for binding by the transcription factor nerve growth factor induced protein A (NGFI-A), which is involved in neuronal plasticity. In rats, it has been shown that individuals less susceptible to depressive ...
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]
It has been observed that the pathology of depression involves dysfunction of monoamine neurotransmitter circuits in the CNS, particularly of serotonin and norepinephrine. Selective serotonin reuptake inhibitors (SSRIs) are the most widely used antidepressant and include fluoxetine (Prozac), citalopram (Celexa), and fluvoxamine (Luvox). These ...
5-Hydroxytryptamine receptor 2B (5-HT 2B) also known as serotonin receptor 2B is a protein that in humans is encoded by the HTR2B gene. [ 5 ] [ 6 ] 5-HT 2B is a member of the 5-HT 2 receptor family that binds the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT).
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]
Individuals with the BDNF Val66Met polymorphism are more susceptible to depression, anxiety and bipolar disorder. [4] Furthermore, people with these gene have been found to have decreased hippocampal volume, which is a common structural change associated with depression. This genes results in decreased activity-dependent secretion of BDNF.