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Brain Res Dev Brain Res. 1994 May 13;79(1):136-9.

Differential ontogenetic appearance and regulation of stimulatory G protein isoforms in rat cerebral cortex by thyroid hormone deficiency.

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Section of Biochemical Psychiatry, Clarke Institute of Psychiatry, Toronto, Ontario, Canada.


We have examined the effects of perinatal hypothyroidism on the levels of several G protein subunits in developing rat cerebral cortex. Thyroid deficiency significantly reduced the levels of the short form of G alpha s (G alpha s-s) by 70% and 83%, on P17 and P22, respectively, but had no effect on the long form of G alpha s (G alpha s-1), except that the G alpha s-1 levels were moderately increased on P22. Compared with age-matched controls, no significant differences were observed for G alpha i-1, G alpha i-2, G alpha o, G alpha q/11, G beta 1 and G beta 2 immunoreactivity in the cerebral cortex of the 22-day-old hypothyroid pups. These findings suggest that thyroid hormones may play an important role in controlling the pattern of expression of G alpha s isoforms during neonatal brain development and the reduced levels of G alpha s-s may contribute to some of the developmental abnormalities seen with perinatal hypothyroidism by altering signal transduction and intercellular communication.

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