دانلود مقاله ISI انگلیسی شماره 69530
عنوان فارسی مقاله

ناهمسانی استرس مزمن گلوکوکورتیکوئید واکنش بازخورد منفی در موش را تنظیم می کند

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
69530 2001 17 صفحه PDF سفارش دهید محاسبه نشده
خرید مقاله
پس از پرداخت، فوراً می توانید مقاله را دانلود فرمایید.
عنوان انگلیسی
Chronic stress differentially regulates glucocorticoid negative feedback response in rats
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Psychoneuroendocrinology, Volume 26, Issue 5, July 2001, Pages 443–459

کلمات کلیدی
استرس مزمن؛ کورتیکوسترون؛ آزمون دگزامتازون؛ بازخورد منفی گلوکوکورتیکوئید؛ گلوکوکورتیکوئید؛ هیپوکامپ
پیش نمایش مقاله
پیش نمایش مقاله ناهمسانی استرس مزمن گلوکوکورتیکوئید واکنش بازخورد منفی در موش را تنظیم می کند

چکیده انگلیسی

Exposure to chronic stress is thought to play an important role in the etiology of depression. In this disorder, a disrupted negative feedback response to exogenous glucocorticoids on cortisol secretion has been indicated. However, the regulation of glucocorticoid negative feedback by chronic stress is not fully understood. In the present study, we investigated the effects of chronic stress administered by water immersion and restraint (2 h/day) for four weeks on the glucocorticoid feedback in rats. In the acutely (one-time) stressed rats, the basal plasma corticosterone (CORT) level was markedly elevated, remained at high levels for 5 h after the termination of stress, and then decreased. In the chronically stressed rats, the CORT level was initially elevated similarly, but rapidly decreased at 2 h. In the dexamethasone (DEX) suppression test, the peak CORT level in response to stress was not suppressed by DEX in the acutely stressed rats, but was significantly suppressed in the chronically stressed rats. In contrast, the suppressive effects of DEX on the basal CORT secretion in naive rats were attenuated in the chronically stressed rats. In the chronically stressed hippocampus, which plays an important role in the regulation of the glucocorticoid feedback response, the binding of [3H]DEX was decreased and the increased response of activator protein-1 induced by acute stress was abolished. These results suggest that chronic stress induces a hypersuppressive state for induced CORT secretion in response to acute stress, which is caused by partial habituation, coping, and adaptation to the stressor, whereas it induces a hyposuppressive state for the basal CORT secretion, which is caused by glucocorticoid receptor downregulation. These mechanisms may be involved in the stress-induced neural abnormalities observed in depression.

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