PubMed · 13652976
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M SKALKA. 1959-04-15. [Adrenal function & liver changes after x-irradiation].. https://doi.org/10.1007/bf02165536
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Male rats outperform females in spatial tasks, such as the water maze (WM). Female rats are known to have higher basal serum corticosterone (CORT) levels and to manifest a more rapid and stronger CORT response to novel stressors. Sex differences in stress responses to the handling and forced swimming in the WM task might contribute to the sex difference in WM performance. In Experiment 1, naive females were found to be impaired relative to naive males in swimming to a visible platform in a WM pool due to strongly thigmotaxic swimming by females. In Experiment 2, serum CORT, a physiological measure of stress, was highly elevated during and after WM training, with female > male values and strong inverse correlations between CORT and measures of WM performance in females. Familiarization with the WM pool and test procedures by strategies pretraining prior to spatial training reduced or eliminated the sex differences in the stress response and WM performance. In Experiment 3, adrenalectomy to eliminate the stress response eliminated sex differences in WM performance. Taken together, the results suggest that male and female rats may harbor brain circuitry that is equally capable of accurate spatial navigation and memory in the WM but which may be impaired to different degrees by the differential stress responses triggered by WM testing.
In previous studies examining the role of glucocorticoids and thyroid hormone on the maturation of the Na(+)/H(+) antiporter (NHE3), we found attenuation in the maturational increase in proximal tubule apical Na(+)/H(+) antiporter activity but no change in NHE3 mRNA abundance in either glucocorticoid-deficient or hypothyroid rats. In addition, prevention of the maturational increase in either hormone failed to totally prevent the maturational increase in Na(+)/H(+) antiporter activity. We hypothesized that one hormone played a compensatory role when the other was deficient. The present study examined whether combined deficiency of thyroid and glucocorticoid hormones would completely prevent the maturation of the Na(+)/H(+) antiporter. Adrenalectomy was performed in 9-day-old hypothyroid Sprague-Dawley rats, a time before the normal postnatal maturational increase in these hormones occurs. Nine- and 30-day-old adrenalectomized (ADX), hypothyroid rats had comparable NHE3 mRNA abundance, which was 5- to 10-fold less than 30-day-old ADX, hypothyroid rats that received corticosterone-thyroxine replacement and 30-day-old sham control rats (P < 0.05). Brush-border membrane NHE3 protein abundance was comparable in 9- and 30-day-old ADX, hypothyroid groups and approximately 20-fold lower than both the 30-day replacement and 30-day sham groups (P < 0.05). Similarly, the replacement and sham groups had higher sodium-dependent proton secretion than 9- and 30-day-old ADX, hypothyroid groups (P < 0.05). We conclude that combined deficiency of both hormones totally prevents the maturational increase in NHE3 mRNA and protein abundance and Na(+)/H(+) antiporter activity.
Previous work has shown that glucocorticoids accelerate splenic T cell proliferation in vitro. To test whether chronic exposure to high levels of glucocorticoids in vivo would affect this accelerating effect, we offered adrenalectomized rats a high dose of corticosterone (CORT; 150 microg/ml in saline), a physiological replacement dose of CORT (15 microg/ml in saline), or saline to drink. We also included a group of sham-adrenalectomized rats. After 1 wk of treatment, splenic lymphocytes of these animals were cultured in the presence or the absence of 1000 nm CORT. The central finding was that the CORT-evoked acceleration of the proliferative response in vitro was attenuated in splenic T cells from animals that had received the high-dose CORT treatment in vivo. This observation could not be explained by changes in IL-2 levels in culture supernatants, the cellular composition of the spleens, or an altered glucocorticoid receptor expression in T cells. As a candidate mechanism, we identified the abrogation of a CORT-evoked enhancement of IL-2 receptor expression. This finding underscores the pivotal role of the IL-2 receptor in the modulation of cellular immunity by glucocorticoids. We conclude that the attenuated acceleration of T cell proliferation after long-term exposure to elevated glucocorticoid levels may underlie the well-known impairment of immune function under chronic stress.