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ABSTRACT
Persistent effects of stress were found in second generation rats bred from females whose own mothers had been stressed during pregnancy. The second generation rats grew more slowly, with a plateau in the growth being reached at the same age as in the controls. This resulted in adult animals of both sexes being permanently smaller than their control counterparts. When these offspring were subjected to short-term stress (one session) in adulthood, the response was not significantly different to that for the controls, indicating an intact emergency response. The male offspring from the stressed group, however, had a significantly (P < 0·01) higher plasma progesterone concentration, and a significantly (P < 0·01) lower testicular enzymic 3β-hydroxysteroid dehydrogenase activity at rest, when compared with the control offspring. The fertility of the mature female from the stressed group was not affected as a third generation of litters born did not differ from the controls.
It is suggested that a changed genetic programme in the ovarian germ cells of the first generation and/or a changed uterine environment in the second generation may be implicated.
J. Endocr. (1986) 109, 239–244
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Search for other papers by SEYMOUR KESSLER in
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SUMMARY
The development of the pituitary-adrenocortical stress response was studied in CBA/J × DBA/2J hybrid mice. On the basis of the plasma corticosterone response 15 min after a subcutaneous injection of histamine dihydrochloride (50 mg/kg), the first three neonatal weeks could be divided into stress-nonresponsive (3–211 days) and stress-responsive 16–21 days) periods. During the former period, corticosterone levels in the brains of the non-stressed control mice were 63% higher than those of comparable mice during the latter period. Histamine stress significantly increased corticosterone concentrations in the brain during both these periods, but the increase was much greater (88%) during the stress-responsive period than during the stress-nonresponsive period (29%).
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ABSTRACT
The response of prolactin to chronic stress in intact, adrenalectomized and adrenomedullectomized male rats was studied. Immobilization stress in intact animals induced a significant increase in plasma concentrations of prolactin after 20 and 45 min and a significant decrease when the rats were submitted to chronic restraint (6 h daily for 4 days). Five weeks after adrenomedullectomy, plasma prolactin and corticosterone responses to chronic stress were not modified. In contrast, the inhibitory effect of chronic stress on prolactin secretion was totally suppressed by adrenalectomy. When treated with dexamethasone during the 4 days of restraint, adrenalectomized stressed rats showed similar plasma concentrations of prolactin to the intact stressed rats. These data indicate that the adrenal cortex is able to play an inhibitory role on prolactin secretion during stress only through a prolonged release of glucocorticoids.
Journal of Endocrinology (1989) 120, 269–273
Division of Applied Medicine, Department of Anatomical Sciences, School of Medical Sciences, School of Veterinary Medicine and Science, UMR 1198, Institute of Medical Sciences, Centre for Reproductive Endocrinology and Medicine, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK
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versus P12 P20 versus P16 P12 versus C12 P16 versus C16 P16 versus C12 Structural proteins VIM 1 53.8 5.06 828 P48616 +7.89 +2.75 −2.53 −1.67 −4.81 +1.63 7 52.9 5.10 156 LMNA 584 12.1 9.02 330 Q3SZI2 −1.87 +1.05 +1.41 −1.46 +1.35 −1.38 Oxidative stress
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. 1995 , Kishi et al . 1999 , Obrosova et al . 2005 b ) and oxidative stress is increased within the sciatic nerve and the dorsal root ganglia (DRG) containing the sensory neuron cell bodies ( Vincent et al . 2004 ). It is also established that all
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In addition to its known effects on keratinocyte proliferation and differentiation, the hormonal form of vitamin D, 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), has been shown to protect keratinocytes from UV- and chemotherapy-induced damage. Epidermal keratinocytes contain both the machinery needed to produce 1,25(OH)(2)D(3) and vitamin D receptors. The activation of the stress-activated protein kinases (SAPKs), such as c-Jun N-terminal kinase (JNK) and p38, is an early cellular response to stress signals and an important determinant of cell fate. This study examines whether modulation of these SAPKs is associated with the effects of 1,25(OH)(2)D(3) on keratinocytes under stress. HaCaT keratinocytes were exposed to heat shock, hyperosmotic concentrations of sorbitol, the epidermal growth factor receptor tyrosine kinase inhibitor AG1487, the pro-inflammatory cytokine tumor necrosis factor alpha, and H(2)O(2). These stresses activated both SAPKs. Pretreatment with 1,25(OH)(2)D(3) inhibited the activation of JNK by all stresses and the activation of p38 by heat shock, AG1478 and tumor necrosis factor alpha. Under the same conditions, treatment with 1,25(OH)(2)D(3) protected HaCaT keratinocytes from cytotoxicity induced by exposure to H(2)O(2) and hyperosmotic shock. The effect of 1,25(OH)(2)D(3) was dose-dependent, already apparent at nanomolar concentrations, and time-dependent, maximal after a 24-h pre-incubation. We suggest that inhibition of SAPK activation may account for some of the well-documented protective effects of 1,25(OH)(2)D(3) on epidermal cells during exposure to UV or chemotherapy and may also be related to the anti-inflammatory actions of the hormone in skin.
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Wolfson Laboratory for Research in Gerontology, Department of Zoology, University of Hull, Hull, HU6 7RX
(Received 20 June 1977)
A relative lack of adrenocortical responsiveness to stress has been described in the rat during the period from day 2 to about day 16 of neonatal life (Schapiro, Geller & Eiduson, 1962; Levine, Glick & Nakane, 1967; Corte & Yasumura, 1975) and the reports to date seem to implicate a lack of response of the pituitary gland as the primary cause (Zarrow, Philpott & Denenberg, 1968; Donovan, 1970; Corte & Yasumura, 1975). Since very little work has been done on the response of the pituitary gland to stress in the neonatal rat, the present study was undertaken.
Female Sprague–Dawley rats weighing 300 g were housed at 22 °C with a light : darkness cycle of 12 : 12 h. Mated female rats were isolated on day 1 of pregnancy, and after
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ABSTRACT
Ether stress applied at 10.00 h induced a 100% increase in serum prolactin in intact and ovariectomized androgenized rats. Ovariectomy significantly diminished the basal serum prolactin values observed in intact androgenized rats. Two doses of progesterone (5 mg) given to intact and ovariectomized androgenized rats 14 and 2 h before exposure to ether stress increased prolactin values in the control groups but completely prevented the effect of stress. Exposure to ether stress induced a 100% increase in serum prolactin values in androgenized rats with increased serum progesterone levels 4 days after the induction of ovulation and the luteal phase with human chorionic gonadotropin (hCG). A group of androgenized rats with induced maternal behaviour and which had been suckled for 6 days was given 100 i.u. hCG and suckled for another 6 days after the hCG-induced luteal phase had been established. The serum prolactin and progesterone values of these rats were significantly higher than those treated with hCG only and ether stress did not increase prolactin release. A greatly increased serum concentration of prolactin was obtained in pro-oestrous and oestrous virgin rats after exposure to ether stress. Serum prolactin was also increased by stress in male rats. Progesterone administration to these female and male rats prevented stress-induced prolactin release. To ascertain the part played by dopamine and serotonin in the effect of stress on prolactin release, groups of androgenized and oestrous female rats were treated with bromocriptine or p-chlorophenylalanine methylester hydrochloride (pCPA). The dopaminergic agonist bromocriptine markedly reduced prolactin levels in the unstressed androgenized rats, but did not prevent the prolactin increases induced by stress. Administration of pCPA had no effect on basal or stress-increased serum levels of prolactin. It is concluded that modifications of the ovarian steroid secretions, especially of progesterone, has profound effects on prolactin release in response to ether stress. The release of the hormone was not mediated by a dopaminergic or serotonergic regulatory pathway.
J. Endocr. (1986) 110, 423–428
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SUMMARY
The effects of four types of stress (daily subcutaneous injection of 0·9 % NaCl solution, a forced choice, water gavage, and surgical trauma) on the growth rate, food and water intake, and water excretion of albino rats have been investigated. These stresses caused a slowing of growth which was apparently not associated with decreased food and water intakes. There were, however, some changes in water excretion which varied with the type of stress. Since food consumption was unchanged during stress whereas the rate of growth decreased it is concluded that the rate of oxidative metabolism was increased.
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ABSTRACT
Pituitary-adrenal, pituitary-gonadal and prolactin responses to acute stress (restraint) were studied in peripuberal and adult male rats. The pituitary-adrenal response to restraint stress did not differ in peripuberal and adult rats. Prolactin increase during stress was less marked in peripuberal animals. While an increase in LH during stress was observed in adult rats, peripuberal animals did not respond to stress. Testosterone levels were also lower in peripuberal than in adult rats. Diminished LH and prolactin responses to stress in peripuberal rats did not appear to be due either to increased pituitary-adrenal activity or to altered pituitary responsiveness to LHRH and dopamine respectively. Peripuberal rats were also more sensitive to the action of morphine on LH and prolactin release than were adult rats, suggesting that endogenous opioids may be involved in the LH and prolactin responses to acute stress. Differences in the maturation of central mechanisms rather than in pituitary response appear to be responsible for the differing responses to acute stress.
J. Endocr. (1987) 112, 9–13
