[A study on developmental characteristics of optic nerve in a rat model of materno-foetal hypothyroidism]

It is well known that vertebrates Central Nervous System reacts to a wide variety of hormones, and growth factors. However the basic maturation mechanisms and remodelling processes remain in general unknown. Thyroid hormones tri-iodothyronine (T(3)) and thyroxine (T(4)) modulate this metabolism, playing a role in cell differentiation and proliferation and in gene expression during growth. The aim of the present study was to investigate whether or not low levels of thyroid hormone in blood, obtained with an experimental model of congenital neonatal hypothyroidism referred to herein, may induce changes in optic nerve development, mainly in processes of macroglial cell genesis and myelination.

We used an experimental model of materno-foetal hypothyroidism (MFHP) set up in a rat through chemical thyroidectomy. A solution of methyl-mercapto-imidazole and KClO(4) was administered with drinking water to pregnant rats and their offspring during gestation and lactancy. A group of rats was maintained in parallel as controls (C-G). Optic nerves were excised from both groups at key postnatal developmental stages (P) and these were prepared for light and transmission electron microscopy.

Cross-sectional areas of optic nerves in the MFHP-G group appeared significantly smaller compared to C-G, this, during the perinatal phase as well as P25 (p<0.01). Macroglial cell nuclear cross-sectional areas showed increasing values in both groups. Data from MFHP-G, however, showed significantly lower than those of C-G (p<0.01). Between 4 to 6 days delayed myelination was at all times observed in the treated group.

All results suggest that T(3) and T(4) regulate optic nerve development by stimulating glial cells function at cell nuclear level, probably through specific receptor binding sites, as suggested in earlier literature (Pinazo-Durán et al. Arch. Soc. Esp. Oftalmol., 1997).