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首页> 外文期刊>Psychoneuroendocrinology: An International Journal >Neuroendocrine stress reactivity of male C57BL/6N mice following chronic oral corticosterone exposure during adulthood or adolescence
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Neuroendocrine stress reactivity of male C57BL/6N mice following chronic oral corticosterone exposure during adulthood or adolescence

机译：慢性口服皮质酮暴露于成年或青春期后雄性C57BL / 6N小鼠的神经内分泌应激反应性

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Highlights ? Chronic oral corticosterone during adulthood or adolescence leads to somatic and neuroendocrine changes in male mice. ? Adolescent-treated males show weight loss during corticosterone exposure, an effect not observed in adult-treated males. ? Oral corticosterone results in dampen hormonal stress reactivity, independent of age of treatment. ? Stress-induced neural activation in the PVN occurred in both adult- and adolescent-treated animals. Abstract Adolescence is associated with the maturation of the hypothalamic-pituitary-adrenal (HPA) axis, the major neuroendocrine axis mediating the hormonal stress response. Adolescence is also a period in development marked by a variety of stress-related vulnerabilities, including psychological and physiological dysfunctions. Many of these vulnerabilities are accompanied by a disrupted HPA axis. In adult mice, a model of disrupted HPA function has been developed using oral chronic corticosterone administration via the drinking water, which results in various physiological and neurobehavioral abnormalities, including changes in stress reactivity and anxiety-like behaviors. In an effort to further complement and extend this model, we tested the impact of HPA disruption in adolescent mice. We also examined whether this disruption led to different outcomes depending on whether the treatment happened during adolescence or adulthood. In the current set of experiments, we exposed adult (70days of age) or adolescent (30days of age) male C57BL/6N mice to 4 weeks of either 0 or 25μg/ml oral corticosterone via their drinking water. We measured body weight during treatment and plasma corticosterone levels and activation of the paraventricular nucleus (PVN), as indexed by FOS immunohistochemistry, before and after a 30min session of restraint stress. Our data indicate that adolescent animals exposed to chronic corticosterone showed weight loss during treatment, an effect not observed in adults. Further, we found stress failed to elevate plasma corticosterone levels in treated mice, regardless of whether exposure occurred in adulthood or adolescence. Despite this reduced hormonal responsiveness, we found significant neural activation in the PVN of both adult- and adolescent-treated mice, indicating a dissociation between stress-induced peripheral and central stress responses following chronic corticosterone exposure. Moreover, stress-induced neural activation in the PVN was unaffected by chronic corticosterone treatment in adult animals, but led to a hyper-responsive PVN in the corticosterone-treated adolescent animals, suggesting an age-specific effect of corticosterone treatment on later PVN stress reactivity. Together, these experiments highlight the influence of developmental stage on somatic and neuroendocrine outcomes following chronic HPA disruption by noninvasive, oral corticosterone treatment. Given the substantial vulnerabilities to HPA dysfunctions during adolescence this model may prove useful in better understanding these vulnerabilities.
机译：强调 ？在成年期或青春期期间的慢性口腔皮质酮导致雄性小鼠的体细胞和神经内分泌发生变化。还青少年治疗的雄性在皮质酮暴露过程中显示出体重减轻，在成人处理的男性中未观察到的效果。还口服皮质酮导致抑制激素应激反应性，与治疗年龄无关。还在成人和青少年治疗的动物中，PVN中的应激诱导的神经活化发生。摘要青春期与下丘脑 - 垂体 - 肾上腺（HPA）轴的成熟有关，主要神经内分泌轴介导荷尔蒙应激反应。青春期也是一种开发的时期，标志着各种与压力相关的脆弱性，包括心理和生理功能障碍。这些漏洞中的许多伴随着中断的HPA轴。在成人小鼠中，使用饮用水口服慢性皮质酮给药开发了破坏的HPA功能模型，这导致各种生理和神经兽性异常，包括压力反应性和焦虑的行为的变化。为了进一步补充和扩展该模型，我们测试了HPA中断在青少年小鼠中的影响。我们还检查了这种中断是否导致不同的结果，这取决于治疗是否发生在青春期或成年期间。在目前的实验中，我们通过其饮用水将成人（70天）或青少年（年龄为70天）或青少年（30天）的青少年（年龄）至0或25μg/ ml口服皮质酮的4周。在治疗期间测量体重和血浆皮质酮水平和椎间盘核（PVN）的激活，如FOS免疫组织化学，在30分钟的约束应激胁迫之前和之后。我们的数据表明，暴露于慢性皮质酮的青少年动物在治疗过程中显示出体重减轻，在成人中未观察到效果。此外，我们发现压力未能升高治疗小鼠中的血浆皮质酮水平，无论是否在成年或青春期发生。尽管荷尔蒙反应性降低，但我们发现了成人和青少年处理的小鼠的PVN中的显着神经激活，表明慢性皮质酮暴露后应力诱导的外周和中央应力反应之间的解离。此外，PVN中的应力诱导的神经活化未受成人动物中的慢性皮质酮处理的影响，但在皮质酮处理的青少年动物中导致了过度响应的PVN，表明皮质酮处理对后来的PVN应力反应性的年龄特异性效果。这些实验在一起突出了慢性HPA破坏慢性，口服皮质酮治疗后慢性HPA破坏的发展阶段对体细胞内分泌结果的影响。鉴于青春期期间对HPA功能障碍的大量漏洞此模型可能证明可以更好地理解这些漏洞。

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