Effect of maternal hypothyroxinaemia during fetal life on the calmodulin-regulated phosphatase activity in the brain of the adult progeny in the rat

Abstract

Calmodulin-regulated phosphatase activity was measured in the brain of 2-month-old rats born from hypothyroid and normal dams, using a fluorometric enzyme assay developed for this purpose. Calmodulin content was measured in the same brain regions by radioimmunoassay. Significant differences between groups in weight and protein content, basal phosphatase and calmodulin-regulated phosphatase activity were found. The brain region most affected was the cerebellum, where basal and calmodulin-regulated phosphatase activities, and protein content were increased. The data point towards a lasting effect of maternal hypothyroxinaemia on the brain function of the progeny.

Hypothyroidism selectively reduces the rate and amount of transport for specific SCb proteins in the hyt/hyt mouse optic nerve

“…Elevated calmodulin may also act on membrane proteins, second messenger pathways, and metabolic pathways. These results are consistent with previous observations that may link depressed levels of brain T3 (triiodothyronine) in the progeny of maternal hypothyroidism (Porterfield and Hendrich,199 1) with increases in calmodulin-related phosphatase activity in the brains of these progeny (Ruiz de Elvira et al, 1989).…”

Maternal hypothyroxinaemia during the first half of gestation in an iodine deficient area with endemic cretinism and related disorders

“…Neurobiological and behavioural effects of maternal hypothyroxinaemia during pregnancy in animal models have been definitely elucidated in rats in numerous studies (Ruiz de Elvira et al, 1989;Hadjzadeh et al, 1990;Sinha et al, 1992;Attree et al, 1992) and in the sheep (Hetzel & Potter, 1983;Potter et al, 1986). Therefore, maternal thyroid hormone transfer to the fetus, previously denied or considered of minimal relevance (Fisher & Klein, 1981;Roti et al, 1983) but recently demonstrated in rats (Escobar del Rey et al, 1986;Woods et al, 1984) and inman (Vulsma et al, 1989) appears to be of critical importance in intrauterine brain development.…”

Maternal and Fetal Thyroid Function

“…The administration of serum from rats with either hypothyroidism or hyperthyroidism induces malformations in rat-embryo cultures in vitro 51 . Finally, the progeny of pregnant rats with hypothyroidism, when studied as adults, have abnormalities in brain amino acid metabolism, marker enzymes of neuronal and glial cells, and calmodulin-regulated phosphatase activity, although postnatal growth and brain weight are not altered 52,53,54 .…”