Plasma glucocorticoid elevation and desynchronization of the estrous cycle following unpredictable stress in the rat

Pollard, Irina; White, Barbara M.; Bassett, J.R.; Cairncross, K.D.

doi:10.1016/s0091-6773(75)90374-0

Cited by 64 publications

(34 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…During proestrous in the rat, hlgher B levels oceur in response to stress than during diestrous and eStrOUS (Pollard et al;1975, Dean et al, 1969. F, as weil as catecholaminergie responses to stress also vary as a function of menstrual phase (Collins et al;1985, Hastrup and Light;1984, Marinari et al, 1976.…”

Section: Hpa-hpg Interactionsmentioning

confidence: 99%

Variations in the Hypothalamic-Pituitary-Adrenal Response to Stress during the Estrous Cycle in the Rat

1991

View full text Add to dashboard Cite

ABSTRACfTo investigate the role of gonadal steroids in the hypothalamic-pituitary-adrenal (HPA) response to stress, we studied adrenocorticotrophin (ACIlI) and corticosterone (B) responses to 20 min re~traint stress in cycling female rats, and in ovariectomized (OVX) rats replaced with physiologicallevels of estradiol (E2) and progestefCIne (P). In cycling rats, we found significantly iligher peak ACfH (p < 0.01) and B (p < 0.05) responses to stress during proestrous compared to the estrous and diestrous phases. No differences were found in either basal ACIH and B levels across the cycle phases. In a seperate study, OVX rats were rnaintained on low, physiologicallevels ofE2 and P with silas tic implants for three days, and injected either with oil (0'), 10 ug of E2 (E') 24 h befon' stress testing, or with E2 and 500 ug P 24 h and 4 h, respectively, prior to stress (EP'). These treatments mimicked endogenous profiles of E2 and P occurine during diestrous, proestrous, and late proestrous-early estrous phases, respectively. In response to stress, ACfH levels were higher (p < 0.01) in the E' group compared to the EP' and 0' groups. Although the peak B response was similar in aIl groups, the E' and EP' groups secreted more B following the termination of stress than did the 0' group. Within the 20 min stress period, ACfH levels in the E' group were significantly (p < 0.05) higher at 5, 10, and 15 min after the onser of stress, compared to the EP' and 0' groups. Plasma B levels were significantly higher in the E' group at 5 and 10 min (p < 0.05 and p < 0.01, respectively) compared to the EP' and 0' group. B-endorphin-like immunoreactive responses to restraint stress were aiso significanùy higher in the E' group compared to the EP' (p < 0.05) and 0' (p < 0.01) groups. There was no effect of E2 on ACfH clearance. These results indicate that the HPA axis in the femate rat is most 11 sensitive to stress during proestrous. Such enhanced HPA responses to stre~,s are limitcd to the early portion of proestrous, as progesterone appears to inhibit the tacilitatory effects of estrogen on ACTH release during stress. Taken together. these results suggest an ovarian influence on both activatonal and inhibitory components of HPA activity.Nous avons investi gué le rôle des stéroides ovariens dans la réponse de l'axe hypothalamo-hypophyso-surrénalien (HPA) aux stress. Pour ceci, la réponse de

show abstract

Section: Hpa-hpg Interactionsmentioning

confidence: 99%

Variations in the Hypothalamic-Pituitary-Adrenal Response to Stress during the Estrous Cycle in the Rat

1991

View full text Add to dashboard Cite

show abstract

“…The effect of stress on strategy use of female mice has not been investigated so far. The strategy of females during stress is of interest because of their higher basal and stress-induced corticosterone concentrations [9][10][11][12][13][14] than observed in male rats. In addition, in multiple learning paradigms females behave differently during naive and in stressful situations compared to males [15].…”

Section: Introductionmentioning

confidence: 99%

Stress and estrous cycle affect strategy but not performance of female C57BL/6J mice

Horst

Kentrop

Kloet

et al. 2013

Behavioural Brain Research

View full text Add to dashboard Cite

show abstract

“…This axis involves the coordinated activity of parvicellular neurons in the hypothalamic paraventricular nucleus (PVN), adrenocorticotropic hormone (ACTH)-secreting corticotropes in the anterior pituitary, and glucocorticoid-secreting cells in adrenal gland to bring together the neuroendocrine response to stress (1,48,55,56). Activity of the HPA axis is markedly influenced by sex steroids, as illustrated by the pronounced elevations in glucocorticoid levels exhibited in female rodents compared with male counterparts (7,45). In ovariectomized (OVX) female rats, estradiol (E 2 ) potentiates the corticosterone response to numerous stressors, including restraint (60).…”

mentioning

confidence: 99%

Estrogen potentiates adrenocortical responses to stress in female rats

Figueiredo

Ulrich‐Lai²,

Choi³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

153

109

View full text Add to dashboard Cite

It is well established that estrogens markedly enhance the glucocorticoid response to acute stress in females. However, the precise mechanism responsible for this regulation is poorly understood. Here, we tested whether estrogens enhance the activation of the paraventricular nucleus (PVN) of the hypothalamus by measuring stress-induced c-fos mRNA expression in the PVN of restraint-stressed ovariectomized (OVX) rats treated with physiologically relevant doses of estradiol (E 2), the major female estrogen. As expected, E2 enhanced plasma corticosterone responses to restraint in OVX females. However, E 2 markedly attenuated the stress-induced c-fos gene expression in the PVN and inhibited plasma ACTH responses in these animals. Furthermore, E 2-inhibitory effects were mimicked by progesterone (P) alone or in combination with E 2. Interestingly, the suppressive central effects of both E 2 and P were apparently independent of basal paraventricular corticotropin-releasing hormone (CRH) transcription, since these ovarian steroids did not significantly affect PVN CRH mRNA expression in unstressed rats. These unexpected findings suggested that E 2 promotes glucocorticoid hypersecretion in females by additional peripheral (i.e., adrenal) mechanisms. Indeed, E 2 markedly enhanced plasma corticosterone responses and adrenal corticosterone content in dexamethasone-blocked OVX rats challenged with varying doses of exogenous ACTH. These results suggest that enhanced adrenal sensitive to ACTH is an important physiological mechanism mediating E 2-related glucocorticoid hypersecretion in stressed females.corticosterone; progesterone; c-fos; adrenal; paraventricular nucleus THE HYPOTHALAMIC-PITUITARY-ADRENAL (HPA) AXIS represents an important output in the neuroendocrine response to stress. This axis involves the coordinated activity of parvicellular neurons in the hypothalamic paraventricular nucleus (PVN), adrenocorticotropic hormone (ACTH)-secreting corticotropes in the anterior pituitary, and glucocorticoid-secreting cells in adrenal gland to bring together the neuroendocrine response to stress (1,48,55,56). Activity of the HPA axis is markedly influenced by sex steroids, as illustrated by the pronounced elevations in glucocorticoid levels exhibited in female rodents compared with male counterparts (7, 45). In ovariectomized (OVX) female rats, estradiol (E 2 ) potentiates the corticosterone response to numerous stressors, including restraint (60). Because E 2 -dependent glucocorticoid hypersecretion to a certain extent parallels elevations in ACTH, it is believed (3, 4) that estrogen acts centrally to modulate the neuroendocrine responses to stress.The central sites and mechanisms responsible for E 2 actions on the stress-induced glucocorticoid surge remain elusive. However, there is evidence that altered neuronal activity in the PVN might be involved in mediating E 2 effects on HPA axis responses to stress. In male rats, systemic injections of E 2 enhance the expression of the immediate early gene c-fos in response to novelty...

show abstract

Plasma glucocorticoid elevation and desynchronization of the estrous cycle following unpredictable stress in the rat

Cited by 64 publications

References 14 publications

Variations in the Hypothalamic-Pituitary-Adrenal Response to Stress during the Estrous Cycle in the Rat

Variations in the Hypothalamic-Pituitary-Adrenal Response to Stress during the Estrous Cycle in the Rat

Stress and estrous cycle affect strategy but not performance of female C57BL/6J mice

Estrogen potentiates adrenocortical responses to stress in female rats

Contact Info

Product

Resources

About