Thyroxine Modulates Corticotropin‐Releasing Factor but not Arginine Vasopressin Gene Expression in the Hypothalamic Paraventricular Nucleus of the Developing Rat

Abstract

Neonatal rats were daily injected with 100 microg/kg T4 and killed at 4, 8 or 15 days. Circulating corticosterone and corticosteroid binding globulin concentrations increased in 8- and 15-day-old rats after T4 treatment. Plasma adrenocorticotropic hormone (ACTH) concentrations, pituitary ACTH content and pro-opiomelanocortin mRNA expression were unaffected in T4-treated rats. T4 treatment induced an increase in corticotropin-releasing factor (CRF) mRNA expression in the whole population of CRF synthesizing cells of the paraventricular nucleus (PVN) that became significant at day 8 and disappeared at day 15. Double labelling in situ hybridization revealed that CRF gene expression in the CRF+/arginine vasopressin (AVP)+ subpopulation was increased at days 4 and 8 and decreased at day 15. CRF immunoreactivity in the zona externa of the median eminence increased with age but was not affected by the experimental hyperthyroidism. The degree of CRF and AVP colocalization, the concentration of AVP mRNA in the parvo and magnocellular cell bodies of the PVN and the density of immunoreactive AVP in the zona interna or zona externa of the median eminence did not change after T4 treatment. Our data demonstrate that experimental hyperthyroidism accelerates the maturation of hypothalamic CRF gene expression, including in particular in the CRF+/AVP+ subpopulation, during the stress hyporesponsive period. These observations suggest that the physiological peak of plasma thyroxine that occurs between days 8-12 may participate in the maturation of hypothalamic CRF cells.

Glucocorticoids, thyroid hormones, and iodothyronine deiodinases in embryonic saltwater crocodiles

“…On days 60 and 68 of development, treatment with T 3 did not affect rT 3 ORD activity in the liver. However, on day 75, treatment with T 3 increased rT 3 ORD activity (P Ͻ 0.05) (Fig. 2A).…”

“…Treatment of embryos with T 3 did not have any effect on rT 3 ORD activity in kidney microsomes (Fig. 2B).…”

“…Effects of hormone treatments on rT 3 ORD activity in liver and kidney microsomes. On days 60 and 68 of development, treatment with T 3 did not affect rT 3 ORD activity in the liver.…”

“…Deiodination is the removal of iodine from iodothyronine molecules. Outer ring deiodination converts T 4 into T 3 and reverse T 3 (rT 3 ) into 3,3Ј-diiodothyronine (T 2 ). Inner ring deiodination converts T 4 into rT 3 and T 3 into T 2 .…”

“…Outer ring deiodination converts T 4 into T 3 and reverse T 3 (rT 3 ) into 3,3Ј-diiodothyronine (T 2 ). Inner ring deiodination converts T 4 into rT 3 and T 3 into T 2 . T 3 is responsible for most of the biological effects of thyroid hormones and is the ultimate ligand for the thyroid hormone receptor (31).…”