Postnatal thyroid hormone supplementation rescues developmental abnormalities induced by congenital-neonatal hypothyroidism in the rat retina.

Thyroid hormones (TH) play a key role in central nervous system development. We have studied the influence of congenital and neonatal hypothyroidism on retinal development and the effects of postnatal TH supplementation. An experimental model was set up using Wistar rats by inducing chemical thyroidectomy during gestation and suckling. Eyes from control (CG) and TH-depleted (THDG) groups of animals were obtained at postnatal days 10 and 25. In the THDG, there was a significant reduction in the retinal thickness and layering, retinal volume, cell number and nuclear volumes in all layers. A third group of rats, made hypothyroid during the gestational and neonatal period and then supplemented with TH (THSG), showed a recovery of both the retinal thickness [at P25: 188.5 +/- 9.2 microm (THSG) vs. 175.8 +/- 16.1 microm (THDG), p < 0.001, and 210.8 +/- 8.9 (CG)] and total retinal cell number [at P25: 6.9 x 10(6) (THSG) vs. 3.7 x 10(6) (THDG) cells, p < 0.001, and 5.3 x 10(6) cells (CG)]. Light and electron microscopy studies confirmed that TH deprivation altered the organization of the retina, which was mostly normalized by hormone administration. Our data show that TH regulates intrinsic mechanisms for controlling retinal cytoarchitecture and layering, and that alterations in retinal maturation induced by congenital-neonatal TH deficiency can be at least partially rescued by early hormonal treatment in vivo.