Co-Expression of c-Fos with Oestradiol Receptor [alpha] or Somatostatin in the Arcuate Nucleus, Ventromedial Nucleus and Medial Preoptic Area in the Follicular Phase of Intact Ewes: Alteration after Insulin-Induced Hypoglycaemia

• Published in: Reproduction in domestic animals Vol. 50; no. 1; p. 68
• Main Authors: Fergani, C, Routly, JE, Jones, DN, Pickavance, LC, Smith, RF, Dobson, H
• Format: Journal Article
• Language: English
• Published: Oxford Blackwell Publishing Ltd 01.02.2015
• Subjects: Animal reproduction; Hormones; Hypoglycemia; Sheep
• ISSN: 0936-6768; 1439-0531
• DOI: 10.1111/rda.12450

Contents The aim of this study was to investigate how acute insulin-induced hypoglycaemia (IIH) alters the activity of cells containing oestradiol receptor [alpha] (ER[alpha]) or somatostatin (SST) in the arcuate nucleus (ARC) and ventromedial nucleus (VMN), and ER[alpha] cells in the medial preoptic area (mPOA) of intact ewes. Follicular phases were synchronized with progesterone vaginal pessaries. Control animals were killed at 0 h or 31 h (n = 5 and 6, respectively) after progesterone withdrawal (PW; time zero). At 28 h, five other animals received insulin (INS; 4 iu/kg) and were subsequently killed at 31 h. Hypothalamic sections were immunostained for ER[alpha] or SST each with c-Fos, a marker of neuronal transcriptional activation. Insulin did not alter the percentage of activated ER[alpha] cells in the ARC; however, it appeared visually that two insulin-treated animals (INS responders, with no LH surge) had an increase in the VMN (from 32 to 78%) and a decrease in the mPOA (from 40 to 12%) compared to no increase in the two INS non-responders (with an LH surge). The percentage of activated SST cells in the ARC was greater in all four insulin-treated animals (from 10 to 60%), whereas it was visually estimated that activated SST cells in the VMN increased only in the two insulin responders (from 10 to 70%). From these results, we suggest that IIH stimulates SST activation in the ARC as part of the glucose-sensing mechanism but ER[alpha] activation is unaffected in this region. We present evidence to support a hypothesis that disruption of the GnRH/LH surge may occur in insulin responders via a mechanism that involves, at least in part, SST cell activation in the VMN along with decreased ER[alpha] cell activation in the mPOA.