Hypothalamic Regulation of Corticotropin-Releasing Factor under Stress and Stress Resilience

This review addresses the molecular mechanisms of corticotropin-releasing factor (CRF) regulation in the hypothalamus under stress and stress resilience. CRF in the hypothalamus plays a central role in regulating the stress response. CRF stimulates adrenocorticotropic hormone (ACTH) release from the...

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Autores principales: Kazunori Kageyama, Yasumasa Iwasaki, Makoto Daimon
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Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/55f403b234e5450db7412a68e7c36684
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spelling oai:doaj.org-article:55f403b234e5450db7412a68e7c366842021-11-25T17:54:43ZHypothalamic Regulation of Corticotropin-Releasing Factor under Stress and Stress Resilience10.3390/ijms2222122421422-00671661-6596https://doaj.org/article/55f403b234e5450db7412a68e7c366842021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12242https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067This review addresses the molecular mechanisms of corticotropin-releasing factor (CRF) regulation in the hypothalamus under stress and stress resilience. CRF in the hypothalamus plays a central role in regulating the stress response. CRF stimulates adrenocorticotropic hormone (ACTH) release from the anterior pituitary. ACTH stimulates glucocorticoid secretion from the adrenal glands. Glucocorticoids are essential for stress coping, stress resilience, and homeostasis. The activated hypothalamic-pituitary-adrenal axis is suppressed by the negative feedback from glucocorticoids. Glucocorticoid-dependent repression of cAMP-stimulated <i>Crf</i> promoter activity is mediated by both the negative glucocorticoid response element and the serum response element. Conversely, the inducible cAMP-early repressor can suppress the stress response via inhibition of the cAMP-dependent <i>Crf</i> gene, as can the suppressor of cytokine signaling-3 in the hypothalamus. CRF receptor type 1 is mainly involved in a stress response, depression, anorexia, and seizure, while CRF receptor type 2 mediates “stress coping” mechanisms such as anxiolysis in the brain. Differential effects of FK506-binding immunophilins, FKBP4 and FKBP5, contribute to the efficiency of glucocorticoids under stress resilience. Together, a variety of factors contribute to stress resilience. All these factors would have the differential roles under stress resilience.Kazunori KageyamaYasumasa IwasakiMakoto DaimonMDPI AGarticleglucocorticoidhypothalamuscorticotropin-releasing factorstressBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12242, p 12242 (2021)
institution DOAJ
collection DOAJ
language EN
topic glucocorticoid
hypothalamus
corticotropin-releasing factor
stress
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle glucocorticoid
hypothalamus
corticotropin-releasing factor
stress
Biology (General)
QH301-705.5
Chemistry
QD1-999
Kazunori Kageyama
Yasumasa Iwasaki
Makoto Daimon
Hypothalamic Regulation of Corticotropin-Releasing Factor under Stress and Stress Resilience
description This review addresses the molecular mechanisms of corticotropin-releasing factor (CRF) regulation in the hypothalamus under stress and stress resilience. CRF in the hypothalamus plays a central role in regulating the stress response. CRF stimulates adrenocorticotropic hormone (ACTH) release from the anterior pituitary. ACTH stimulates glucocorticoid secretion from the adrenal glands. Glucocorticoids are essential for stress coping, stress resilience, and homeostasis. The activated hypothalamic-pituitary-adrenal axis is suppressed by the negative feedback from glucocorticoids. Glucocorticoid-dependent repression of cAMP-stimulated <i>Crf</i> promoter activity is mediated by both the negative glucocorticoid response element and the serum response element. Conversely, the inducible cAMP-early repressor can suppress the stress response via inhibition of the cAMP-dependent <i>Crf</i> gene, as can the suppressor of cytokine signaling-3 in the hypothalamus. CRF receptor type 1 is mainly involved in a stress response, depression, anorexia, and seizure, while CRF receptor type 2 mediates “stress coping” mechanisms such as anxiolysis in the brain. Differential effects of FK506-binding immunophilins, FKBP4 and FKBP5, contribute to the efficiency of glucocorticoids under stress resilience. Together, a variety of factors contribute to stress resilience. All these factors would have the differential roles under stress resilience.
format article
author Kazunori Kageyama
Yasumasa Iwasaki
Makoto Daimon
author_facet Kazunori Kageyama
Yasumasa Iwasaki
Makoto Daimon
author_sort Kazunori Kageyama
title Hypothalamic Regulation of Corticotropin-Releasing Factor under Stress and Stress Resilience
title_short Hypothalamic Regulation of Corticotropin-Releasing Factor under Stress and Stress Resilience
title_full Hypothalamic Regulation of Corticotropin-Releasing Factor under Stress and Stress Resilience
title_fullStr Hypothalamic Regulation of Corticotropin-Releasing Factor under Stress and Stress Resilience
title_full_unstemmed Hypothalamic Regulation of Corticotropin-Releasing Factor under Stress and Stress Resilience
title_sort hypothalamic regulation of corticotropin-releasing factor under stress and stress resilience
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/55f403b234e5450db7412a68e7c36684
work_keys_str_mv AT kazunorikageyama hypothalamicregulationofcorticotropinreleasingfactorunderstressandstressresilience
AT yasumasaiwasaki hypothalamicregulationofcorticotropinreleasingfactorunderstressandstressresilience
AT makotodaimon hypothalamicregulationofcorticotropinreleasingfactorunderstressandstressresilience
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