SFE2005 Oral Communications Thyroid and pituitary (8 abstracts)
Department of Cellular and Molecular Neuroscience, Division of Neuroscience and Mental Health, Imperial College London, London, United Kingdom.
The secretion of prolactin is sexually dimorphic and sensitive to changes in gonadal steroid and glucocorticoid status. Reports that the regulatory effects of glucocorticoids on prolactin release are mediated in part via annexin I (ANXA1, 1), have led us to compare prolactin secretion in ANXA1 knockout (KO) and wildtype (WT) mice and to determine the effects ovariectomy and oestrogen replacement (80 nanograms/0.1 ml, s.c./day) on (a) the plasma prolactin concentration (radioimmunoassay) and (b) the number of tyrosine hydroxylase (TH) positive cells (immunocytochemistry) in the hypothalamic arcuate and periventricular nuclei (AN & PN). There were no differences in plasma prolactin concentration or pituitary prolactin content in ANXA1 KO vs. WT controls. In both strains, ovariectomy suppressed the plasma prolactin concentration and this was reversed by the biologically active oestrogen, 17β-oestradiol, which produced a further elevation in plasma prolactin in WT but not KO animals. There were no significant differences in plasma luteinising hormone (LH) concentrations between ANXA1 KO and WT animals at any stage of the oestrous cycle. ANXA1 gene deletion did not affect TH-positive cell number in the AN or PN. TH-positive cell number in the AN was unaffected by ovariectomy or oestrogen replacement. Ovariectomy did, however, significantly increase (P<0.05) TH-positive cell number in the PN of WT animals which was significantly reduced (P<0.05) by oestrogen replacement. There were no significant changes in TH-positive cell numbers in the PN of ANXA1 KO animals following ovariectomy or hormone replacement.
The results suggest that ANXA1 gene deletion causes alterations the sensitivity of the hypothalamo-pituitary prolactin axis to oestrogen. In addition, oestrogen exerts differential effects on TH expression in the PN and AN. The interactions of ANXA1 and gonadal factors in the regulation of prolactin release require further study.
1. John CD et al (2004). TEM 15, 103–109.
Generously supported by the Wellcome Trust.