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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.
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]
Serotonin's presence in insect venoms and plant spines serves to cause pain, which is a side-effect of serotonin injection. [21] [22] Serotonin is produced by pathogenic amoebae, causing diarrhea in the human gut. [23] Its widespread presence in many seeds and fruits may serve to stimulate the digestive tract into expelling the seeds.
NHS figures show that the number of people in England taking antidepressants continues to rise, with 8.3m patients receiving them in 2021/22.
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 ...
The receptor in question is part of the serotonin system, which plays an important role in regulating involuntary body functions like heart rate, breathing and blood pressure.
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 ...
Chemoreceptor activity, however, also affects cardiovascular function either directly (by interacting with medullary vasomotor centers) or indirectly (via altered pulmonary stretch receptor activity).
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