Shift in Adenohypophyseal Activity during Chronic Intermittent Immobilization of Rats

Abstract

Female rats were subjected to 8 h of daily immobilization for 1, 3, 6, 10 or 15 days. Exposure for 3 days inhibited b.w. and induced adrenal enlargement as well as thymus involution; 6 days of stress elicited atrophy of the ovaries and hypophysis. During the later stages of the experiment, the animals showed a positive metabolic balance, and the initial weight alterations of the endocrine glands either tended to regress or were stabilized. On the 6th day, plasma corticosterone reached a peak which was maintained until the end of the experiment, whereas growth hormone (GH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) titers, as determined by radioimmunoassay, fell to 28, 39 and 55% of control values, respectively, following the 1st period of restraint; prolactin (Prl) decreased by 30% after the 3rd day. Thereafter, the plasma concentrations of these hormones remained low, around 40–60% of control levels, although FSH on The 6th day revealed a transient but significant elevation to 180% of initial values. After 15 days of 6-h-daily immobilization, an injection of LH-releasing hormone (LH-RH) and thyrotropin releasing hormone (TRH) induced dramatic increases of LH, FSH, Prl and thyrotropin stimulating hormone (TSH) in plasma. On the basis of the morphologic and hormonal changes, it appears that, in agreement with the concept of a shift in adenohypophyseal activity during severe chronic stress, repeated long-term restraint elicits an inverse relationship between the secretion of ACTH and that of GH, LH, Prl and, to a lesser degree, FSH. Such modifications do not seem to be associated with an inability of the pituitary to secrete these hormones, since it is still responsive to releasing factors.

The Antiglucocorticoid, RU486, Attenuates Stress-Induced Decreases in Plasma-Luteinizing Hormone Concentrations in Male Rats

“…Comparison of different acute stress paradigms by our laboratory and others [3,5] suggests that disparate patterns of LH release during acute stress may reflect, in part, differences in the nature and/or intensity of the stress stimuli employed. Chronic implementation of stress, on either a continuous or intermittent basis, is consistently inhibitory to pituitary LH release [1,2,5,8,[12][13][14][15], Current studies suggest that stress-induced decreases in circulating LH reflect inhibitory mechanisms at the level of the brain and pituitary. Specific neuropeptides and neuro transmitters, including [i-endorphin ((LEND) [16], dynorphin (DYN) [16], corticotropin-releasing factor (CRF) [17], and serotonin [18], have been characterized as com ponents of the neural circuitry by which stress inhibits hypothalamic gonadotropin-releasing hormone (gnRH) re lease.…”

“…Specific neuropeptides and neuro transmitters, including [i-endorphin ((LEND) [16], dynorphin (DYN) [16], corticotropin-releasing factor (CRF) [17], and serotonin [18], have been characterized as com ponents of the neural circuitry by which stress inhibits hypothalamic gonadotropin-releasing hormone (gnRH) re lease. Furthermore, activation of the pituitary-adrenal axis is a consistent physiological response to stress [ 19], and correlations between elevated levels of endogenous or exogenous glucocorticoids and decreased plasma LH con centrations have been reported in rats [1,[20][21][22][23], Gluco corticoids apparently exert direct inhibitory effects on pituitary' gonadolropes since exogenous steroids can sup press GnRH-induced LH release from perifused pituitarytissue in vitro [24,25], The recent localization of glucocor ticoid receptors (GR) within hypothalamic loci pertinent to the regulation of pituitary function [26][27][28][29] support the possibility that these steroids may also act at suprapituitary sites to inhibit LH release during stress. At present, how ever.…”

“…Stress alters the secretion of several anterior pituitary hormones, including luteinizing hormone (LH) [1,2]. Acute stress results in variable patterns of LH release in intact rats: plasma LH levels have been reported to be increased [3][4][5][6][7][8], decreased [3,5,9], or unaltered [10,11] in these animals as a consequence of brief or limited exposure to stress.…”

A stressz és a fertilitás

“…A stresszélettannal foglalkozó tanulmányok sorozatá-ban Selye és munkatársainak 1976-ban jelent meg az a közleménye [9], amelyben állatkísérletekben vizsgálták a stressz és az adenohypophysis hormonjainak összefüggé-sét. Nőstény patkányokat kényszerítettek mozdulatlanságra napi 8 órában, és a plazmában mérték a hormonszint változását 1, 3, 6, 10 és 15 nap után.…”

Antagonism of Type II, but Not Type I Glucocorticoid Receptors Results in Elevated Basal Luteinizing Hormone Release in Male Rats

“…Stress-induced ac tivation of the pituitary-adrenal endocrine axis coincides with decreased pituitary gonadotropin secretion [1][2][3]. Female rats exhibit deviations of estrous cyclicity follow ing implantation of cortisol [4], as well as an attenuation of the preovulatory luteinizing hormone (LH) surge in response to treatment with cortisol or the potent synthetic glucocorticoid, dexamethasone (DEX) [4,5].…”