Melatonin

MELATONIN

Abnormal secretion of melatonin is observed in ASD, with more children tending to have *higher* melatonin secretion. (i.e. see: Chamberlain et al. 1990)

Patients with hypothyroidism were found to have higher peak serum melatonin values, total nocturnal melatonin secretion, and urinary excretion of melatonin than normal individuals (Rojdmark et al, 1991).

Melatonin concentrations were positively correlated with TSH levels in hypothyroidism, and negatively correlated with T3 in hyperthyroidism (Soszynski et al, 1988).

Thyroid hormones were demonstrated to play a role in serotonin metabolism control in the pineal gland. Excess and deficiency of thyroid hormones produce opposite effects in the epiphysis (Rom-Bugoslavskaia et al, 1984)

Under deficiency of thyroid hormones the pathway of oxidative serotonin deamination with primary formation of 5-hydroxyindole-acetic acid (5 HTAA) is the predominant one. Excess and deficiency of thyroid hormones produce opposite effects in the epiphysis. The data obtained not only support the presence of the negative feed-back in the epiphysis-thyroid system but also emphasize that the process of formation of epiphyseal methoxyindoles is the most sensitive one to the action of thyroid hormones (Rom-Bugoslavskaia et al, 1984).

Gq/11: (Bryden et al, 1999)

"We show that Mel 1a receptors functionally couple to both PTX-sensitive and PTX-insensitive G proteins. The previously unknown signaling of Mel 1a receptors through G(q/11) widens the spectrum of potential targets for melatonin."