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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 ...
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 ...
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 ...
In addition, due to their blockade of certain serotonin receptors, serotonergic neurotransmission is not facilitated in unwanted areas, which prevents the incidence of many side effects often associated with selective serotonin reuptake inhibitor (SSRI) antidepressants; [1] [3] hence, in part, the "specific serotonergic" label of NaSSAs. [2]
The exception to this is the 5-HT 3 receptor which is a ligand-gated ion channel. In 2014, a novel 5-HT receptor was isolated from the small white butterfly, Pieris rapae, and named pr5-HT 8. It does not occur in mammals and shares relatively low similarity to the known 5-HT receptor classes. [7]
Serotonin binds a number of receptors, including the 5-HT 3 receptors, which are ligand-gated ion channels that allow the passage of cations in order to depolarize the membrane potential of the postsynaptic neuron that they reside on. [3] Levels of serotonin activity that are lower than normal have been linked to a variety of symptoms ...
Serotonin, in cooperation with a group I metabotropic glutamate receptor (mGluR) agonist, facilitates LTD induction through augmentation of AMPA receptor internalization. This mechanism possibly underlies serotonin's role in the control of cognitive and emotional processes that synaptic plasticity in PFC neurons mediates.
In the brain, serotonin is a neurotransmitter and regulates arousal, behavior, sleep, and mood, among other things. [9] During prolonged exercise where central nervous system fatigue is present, serotonin levels in the brain are higher than normal physiological conditions; these higher levels can increase perceptions of effort and peripheral muscle fatigue. [9]