PubMed · 5091599
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J A Sirs. 1971. Erythrocyte function and aldosterone.. https://doi.org/10.3233/bir-1971-8101
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Prairie voles (Microtus ochrogaster) are monogamous rodents that form pair bonds characterized by a preference for a familiar social partner. In male prairie voles, exposure to either the stress of swimming or exogenous injections of corticosterone facilitate the development of a social preference for a female with which the male was paired after injection or swimming. Conversely, adrenalectomy inhibits partner preference formation in males and the behavioral effects of adrenalectomy are reversed by corticosterone replacement. In female prairie voles, swim stress interferes with the development of social preferences and corticosterone treatments inhibit the formation of partner preferences, while adrenalectomized females form preferences more quickly than adrenally intact controls. Because sex differences in both behavior and physiology are typically reduced in monogamous species, we initially predicted that male and female prairie voles would exhibit similar behavioral responses to corticosterone. However, our findings suggest an unanticipated sexual dimorphism in the physiological processes modulating social preferences. This dimorphic involvement of stress hormones in pair bonding provides a proximate mechanism for regulating social organization, while permitting males and females to adapt their reproductive strategies in response to environmental challenges.
To examine the effect of short-term and long-term adrenalectomy (ADX) on the glucocorticoid receptor (GR) expression, we performed an immunohistochemical study on the rat forebrain. One day after ADX, the GR-immunoreactivity significantly decreased or disappeared in most forebrain structures, while relatively strong GR-immunoreactivity was still found within the hypothalamus especially in the arcuate nucleus (ARC) and the parvocellular paraventricular nucleus (PVN). Two weeks following ADX, GR-immunoreactive cells disappeared in many structures of the forebrain including most parts of hypothalamus while moderate GR-immunoreactivity was still observable in the ARC and PVN. More than 3 months after ADX, the rats still survived when they received replacement of corticosterone during the first 2 weeks following the operation. Moderate GR-immunoreactivity in the ARC and PVN of the hypothalamus was exhibited whereas no immunoreactive cells remained in the cerebral cortex, thalamus and other forebrain structures when these animals showed obvious cell death in the granule cells of the dentate gyrus, identified with the silver impregnation method for degenerating cells. Massive cell loss in this hippocampal region is an indicator of a complete ADX, in addition to the blood corticosterone level. These results demonstrate topographic differences of GR expression in the rat forebrain after ADX with only continuous immunoreactivity in the ARC and PVN of the hypothalamus, suggesting that some neurons in the ARC and PVN could keep active GR probably in order to maintain their survival after removing the adrenal gland.
After discovering that binding to GABAB receptors in rat neocortex varied as a function of the estrous cycle of the rat, we asked whether either or both of the major ovarian steroids could affect binding to GABAB receptors in the same way, namely, by regulating the apparent density (Bmax) of GABAB receptors. We report here that in ovariectomized rats, subcutaneous injection of progesterone alone, without the necessity of estrogen priming, increased the Bmax of baclofen binding to GABAB receptors in the neocortex. Radioimmunoassay of plasma progesterone before and after progesterone injections revealed that plasma progesterone levels similar to those reached during the progesterone surge in proestrus were associated with increased baclofen binding. The effect of progesterone upon baclofen binding was evident 4 h but not 1 h following progesterone treatment. There was some specificity with respect to the cortical receptors affected by progesterone in that under our conditions, progesterone did not increase agonist binding to 5-HT1A or GABAA receptors. We interpret our results to indicate that progesterone variation during the estrous cycle could be responsible for a component of the regulation of GABAB receptors that occurs in neocortex during the estrous cycle of the rat.