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Co‐Expression of c‐Fos with Oestradiol Receptor α or Somatostatin in the Arcuate Nucleus, Ventromedial Nucleus and Medial Preoptic Area in the Follicular Phase of Intact Ewes: Alteration after Insulin‐Induced Hypoglycaemia
Author(s) -
Fergani C,
Routly JE,
Jones DN,
Pickavance LC,
Smith RF,
Dobson H
Publication year - 2015
Publication title -
reproduction in domestic animals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.546
H-Index - 66
eISSN - 1439-0531
pISSN - 0936-6768
DOI - 10.1111/rda.12450
Subject(s) - medicine , endocrinology , arcuate nucleus , somatostatin , insulin , nucleus , periventricular nucleus , follicular phase , hypothalamus , preoptic area , biology , arc (geometry) , chemistry , neuroscience , geometry , mathematics
Contents The aim of this study was to investigate how acute insulin‐induced hypoglycaemia (IIH) alters the activity of cells containing oestradiol receptor α (ER α ) or somatostatin (SST) in the arcuate nucleus (ARC) and ventromedial nucleus (VMN), and ER α cells in the medial preoptic area (m POA ) 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 α or SST each with c‐Fos, a marker of neuronal transcriptional activation. Insulin did not alter the percentage of activated ER α 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 m POA (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 α 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 α cell activation in the m POA .