Kisspeptin, cFos and CRFR Type 2 Coexpression in the Hypothalamus after InsulinInduced Hypoglycaemia

摘要

Normal reproductive function is dependent upon availability of glucose and insulininduced hypoglycaemia is a metabolic stressor known to disrupt the ovine oestrous cycle. We have recently shown that IIH has the ability to delay the LH surge of intact ewes. In the present study, we examined brain tissue to determine: (i) which hypothalamic regions are activated with respect to IIH and (ii) the effect of IIH on kisspeptin cell activation and CRFR type 2 immunoreactivity, all of which may be involved in disruptive mechanisms. Follicular phases were synchronized with progesterone vaginal pessaries and at 28iu h after progesterone withdrawal (PW), animals received saline (niu =iu 6) or insulin (4iu IU/kg; niu =iu 5) and were subsequently killed at 31iu h after PW (i.e., 3iu h after insulin administration). Peripheral hormone concentrations were evaluated, and hypothalamic sections were immunostained for either kisspeptin and cFos (a marker of neuronal activation) or CRFR type 2. Within 3iu h of treatment, cortisol concentrations had increased whereas plasma oestradiol concentrations decreased in peripheral plasma (piu