SFEBES2009 Poster Presentations Neuroendocrinology and behaviour (14 abstracts)
University of Glasgow, Glasgow, UK.
Recent data suggests that oestrogen(E)-responsive somatostatin neurones are involved in the generation of the ovine GnRH surge. Specifically, somatostatin neurones in the hypothalamus are activated (as assessed by nuclear fos) and mRNA levels are elevated in the early stages of the surge induction process. In addition, somatostatin fibres have been visualised in close apposition to hypothalamic GnRH neurones, which may indicate direct neural connection between GnRH and somatostatin neurones. In contrast to normal ewes, those that have been exposed to testosterone during foetal life fail to generate a GnRH surge in response to elevated follicular phase concentrations of E. Whether GnRH neurones possess somatostatin receptors (there are five known subtypes; SSTr1-5) and whether their distribution differs between androgenised and control animals is unknown. Therefore the aim of this study was to map the distribution of SSTr1-5 in the hypothalamus of the normal and the androgenised ewe using immunohistochemistry. To generate androgenised females, pregnant ewes were injected with testosterone propionate (200 mg/week) between day 30 and 90 of gestation (term =147 days). Female control (n=5) and androgenised (n=6) offspring were euthanased at 10 months of age (anoestrus). Hypothalamic sections were obtained to address specific questions: i) are SSTr localised in GnRH neurones?; ii) what type of receptor(s) is it?; and iii) does the distribution of these receptors differ in control v androgenised ewes? SSTr1-5 were all abundant within the preoptic area of the hypothalamus of control and androgenised ewes. However, dual immunohistochemistry demonstrated that GnRH neurones were only immunoreactive for SSTr2. The percentage co-localisation of GnRH neurones and SSTr2 was not significantly different between control and androgenised ewes; 38±10.4 and 42±8.6, respectively. These data indicate that somatostatin may influence GnRH secretion directly via SSTr2. However whether somatostatin plays a role in E positive feedback has yet to be established. Supported by BBSRC.