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Thyroxine Modulates Corticotropin‐Releasing Factor but not Arginine Vasopressin Gene Expression in the Hypothalamic Paraventricular Nucleus of the Developing Rat
Author(s) -
Dakine N.,
Oliver C.,
Grino M.
Publication year - 2000
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.2000.00520.x
Subject(s) - medicine , endocrinology , vasopressin , median eminence , corticotropin releasing hormone , hypothalamus , arginine , colocalization , adrenocorticotropic hormone , corticosterone , population , biology , neuropeptide , gene expression , in situ hybridization , chemistry , hormone , gene , receptor , amino acid , biochemistry , environmental health , microbiology and biotechnology
Neonatal rats were daily injected with 100 μg/kg T 4 and killed at 4, 8 or 15 days. Circulating corticosterone and corticosteroid binding globulin concentrations increased in 8‐ and 15‐day‐old rats after T 4 treatment. Plasma adrenocorticotropic hormone (ACTH) concentrations, pituitary ACTH content and pro‐opiomelanocortin mRNA expression were unaffected in T 4 ‐treated rats. T 4 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 T 4 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.