Journal
MOLECULAR PSYCHIATRY
Volume 6, Issue 6, Pages 647-656Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.mp.4000942
Keywords
corticotropin releasing hormone; CRF; CRH; stress; neonatal; rat; amygdala; paraventricular nucleus; hypothalamus; neuropeptide; glucocorticoids; corticosterone
Funding
- NINDS NIH HHS [R01 NS028912-07A2S1, R01 NS028912-06, NS 28912, R01 NS028912-07A2, R01 NS028912, NS 39307, R01 NS039307, R01 NS039307-01A1] Funding Source: Medline
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Over the last few decades, concepts regarding the presence of hormonal and molecular responses to stress during the first postnatal weeks in the rat and the role of the neuropeptide corticotropin releasing hormone (CRH) in these processes, have been evolving. CRH has been shown to contribute critically to molecular and neuroendocrine responses to stress during development. In turn the expression of this neuropeptide in both hypothalamus and amygdala is differentially modulated by single and recurrent stress, and is determined also by the type of stress (eg, psychological or physiological). A likely transcriptional regulatory factor for modulating CRH gene expression, the cAMP responsive element binding protein CREB, is phosphorylated (activated) in the developing hypothalamus within seconds of stress onset, preceding the transcription of the CRH gene and initiating the activation of stress-induced cellular and neuroendocrine cascades. Finally, early life stress may permanently modify the hypothalamic pituitary adrenal axis and the response to further stressful stimuli, and recent data suggest that CRH may play an integral role in the mechanisms of these long-term changes.
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