Regenerate Serotonin Receptors

Tess Thompson



A receptor is a protein molecule to which a signaling molecule known as ligand can attach. A ligand may be a neurotransmitter, hormone, pharmaceutical drug or a toxin. Ligands may either bind to a receptor for conformational change or simply block it.

Serotonin (also known as 5-hydroxytryptamine or 5-HT) is a monoamine transmitter that has a dual function: that of a neurotransmitter and a peripheral signal mediator. Serotonin receptors are receptors for both these serotonin functions. These are located in the cell membranes and mediate the effects of serotonin. As a neurotransmitter in the central nervous system, serotonin plays a role in mood, anger, aggression, body temperature, sleep and metabolism. In the gastrointestinal tract, it acts as a peripheral signal mediator, and in the blood, it is involved in the constriction of vessels to aid in post-injury healing.

Serotonin activity ceases by its uptake from the synapse, the junction between two neurons. Serotonin receptors work as regulators of serotonin activity. A local feedback mechanism enables cells to increase (upregulate) and decrease (downregulate) the number of receptors to serotonin. This is done to alter the sensitivity of the serotonin to receptors: upregulation is done to increase, while downregualtion is done to decrease sensitivity.

Serotonin receptors not only affect the release and activity of serotonin, but other neurotransmitters as well. Also, increased stimulation of some serotonin receptors can interfere in the therapeutic action of antidepressants and anxiety-relieving drugs. Antidepressants and other drugs used to promote emotional wellness are mainly intended to increase the amount of available serotonin. There is a possibility of these drugs causing over-stimulation of 5HT growth receptors that may cause pulmonary hypertension from pulmonary vasoconstriction.

Postmortem studies of children who die of SIDS (Sudden Infant Death Syndrome) show changes in the serotonin neurons in the brain stem. The evidence is basically anatomical and shows that the number of serotonin cells was doubled and a change in levels of receptors that are involved in homeostatic control occurred. This indicates that deficient serotonin regulation may cause death.

Studies conducted on mice indicate that when expression of a receptor which is responsible for negative feedback was increased, nearly 80% of the mice died. The death, however, was not due to a general failure of body systems, but due to sharp drop in body temperature and an abnormally slow heart rate. The fact that mice were able to survive without serotonin suggests that it is probably the excess of serotonin 5-HT receptors that induces crisis in the human body and not necessarily the level of serotonin itself.

It is important to mention here that not much is know with surety of the role of serotonin and its receptors. Whatever little that is known points towards the number of its receptors being crucial to serotonin levels and the overall emotional health of humans.

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