Stress‐Induced Suppression of Pulsatile Luteinising Hormone Release in the Female Rat: Role of Vasopressin

Abstract

Insulin-induced hypoglycaemic (IIH) stress evokes the release of arginine vasopressin (AVP) and suppresses luteinising hormone (LH) pulses in a number of species, a phenomenon augmented by the presence of oestradiol (E2). The aim of this study was to test the hypothesis that AVP not only disrupts pulsatile LH secretion in the female rat, but specifically mediates the effect of IIH stress on suppressing LH release. The role of E2 in augmenting the disruptive effect of AVP on LH secretion was also addressed. Rats were ovariectomized (OVX) and fitted with intracerebroventricular (i.c.v. ) and intravenous (i.v.) cannulae. For experiments requiring comparisons of neuroendocrine responses in the presence and absence of E2, animals were implanted subcutaneously with E2 or oil-filled capsules respectively. AVP (5 microg) administered via the i.c.v. cannula suppressed LH secretion by decreasing LH pulse amplitude without affecting LH pulse frequency, an effect that was blocked by central administration of an AVP antagonist (25 microg). This inhibitory response was evident only in E2-replaced OVX rats, thus suggesting a sensitizing influence of the gonadal steroid. In the AVP-deficient Brattleboro rats, IIH stress did not interrupt pulsatile LH secretion as demonstrated in Long Evans and Wistar controls. While these data might suggest a pivotal role for AVP in stress-induced suppression of LH release, central administration of an AVP antagonist did not prevent the interruption of LH pulses in response to IIH stress. Furthermore, it would appear that AVP is not primarily involved in hypoglycaemic stress-induced suppression of pulsatile LH secretion since central administration of very high doses of AVP resulted in a suppression of LH pulse amplitude and not frequency, while hypoglycaemic stress caused an interruption of LH pulses.

GPR54-Dependent Stimulation of Luteinizing Hormone Secretion by Neurokinin B in Prepubertal Rats

“…The guide cannula was secured using dental cement (Dental Filling, Swindon, UK), and fitted with a dummy cannula (Plastics One) to maintain patency [31]. Correct cannula placement was confirmed by the observation of gravitational meniscus movement upon insertion of an internal injection cannula (Plastics One) with extension tubing preloaded with artificial cerebrospinal fluid (aCSF).…”

“…On the morning of experimentation, 1 ml normal saline (Animalcare, Dunnington, UK) was intravenously (iv) administered over 10 min and the rats were then attached via the cardiac catheters to a computer-controlled automated blood sampling system, which enables intermittent withdrawal of 30-µl blood samples without disturbing the rats [31]. Once connected, the animals were left undisturbed for 1 h before blood sampling commenced (between 1000 and 1200 h) then blood samples were taken every 5 min for 3 h. After removal of each blood sample, an equal volume of heparinized saline (50 U heparin sodium/ml normal saline; Wockhardt, Wrexham, UK) was infused.…”

Expression of mRNAs Encoding Receptors That Mediate Stress Signals in Gonadotropin-Releasing Hormone Neurons of the Mouse

“…Administration of CRH, vasopressin or interleukin-1 (IL-1) to the medial preoptic area (POA), where the majority of GnRH neurons reside, can alter luteinizing hormone pulsatility [9,10,11]. In a number of cases, a direct link between stress and the production of such modulatory molecules has been demonstrated [11, 12]. Additionally, ultrastructural investigations have suggested that the effects of CRH [13] and glucocorticoid [14] may be direct.…”

Neuroendocrine Control of Gonadotropin Secretion

“…379 In comparing the inhibition of GnRH secretion by stressors with seasonal and lactational effects, it is interesting to note that while stressors are clearly inhibitory in OVX animals, they are generally more effective in the presence of E 2 and/or progesterone than in their absence. [384][385][386][387] These data have usually been interpreted as an action of ovarian steroids to increase the effects of CRH or other mediators of stress, but could equally be viewed as a stressor producing both steroid-independent and steroid-dependent inhibition of GnRH. Recent work in this area has focused on kisspeptin, with the only two papers reporting that endotoxin induced a decrease in Kiss1 mRNA 388 or protein 389 expression in the ARC.…”