Developmental neurobiology of the stress response: Multilevel regulation of corticotropin-releasing hormone function
Developmental neurobiology of the stress response: Multilevel regulation of corticotropin-releasing hormone function
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DOI：
10.1111/j.1749-6632.1997.tb46161.x
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发表时间：
1997-01-01
期刊：
影响因子：
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通讯作者：
Schultz, L
中科院分区：
文献类型：
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作者：
Baram, TZ;Yi, SJ;Schultz, L
In the mature animal, a variety of stressors activate the hypothalamic-pituitary-adrenal (HPA) axis: 1–3 Increased secretion of corticotropin-releasing hormone (CRH) from the hypothalamic paraventricular nucleus (PVN) induces ACTH release from the pituitary and increases plasma corticosterone (CORT). The depletion of hypothalamic CRH is followed by a “compensatory” up-regulation of CRH gene expression. 2–4 Limbic input from hippocampus and amygdala, mainly the central nucleus (ACE), further modulates stressinduced alteration of CRH gene expression. 5, 6The presence of most of these components of the “stress response” in the neonatal (first postnatal week) and infant (second postnatal week) rat has been debated. 7, 8 Elevation of plasma glucocorticoids in response to stressors and the relative roles of CRH and vasopressin have been subjects of investigation. 4, 7–10 A “stress-hypo-responsive” period with diminished or immature hormonal responses has been described during the first two postnatal weeks.
