Journal
FRONTIERS IN NEUROENDOCRINOLOGY
Volume 33, Issue 1, Pages 67-84Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yfrne.2011.08.002
Keywords
Corticotropin releasing hormone (CRH); Hypothalamus; Stress; HPA axis; Transcription; Cyclic AMP response element binding protein (CREB); Transducer of Regulated CREB activity (TORC); Cyclic AMP inducible early repressor ICER; Glucocorticoids
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Funding
- National Institute of Child Health and Human Development
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Corticotropin releasing hormone (CRH) is essential for stress adaptation by mediating hypothalamic-pituitary-adrenal (HPA) axis, behavioral and autonomic responses to stress. Activation of CRH neurons depends on neural afferents from the brain stem and limbic system, leading to sequential CRH release and synthesis. CRH transcription is required to restore mRNA and peptide levels, but termination of the response is essential to prevent pathology associated with chronic elevations of CRH and HPA axis activity. Inhibitory feedback mediated by glucocorticoids and intracellular production of the repressor, Inducible Cyclic AMP Early Repressor (ICER), limit the magnitude and duration of CRH neuronal activation. Induction of CRH transcription is mediated by the cyclic AMP/protein kinase A/cyclic AMP responsive element binding protein (CREB)-dependent pathways, and requires cyclic AMP-dependent nuclear translocation of the CREB co-activator, Transducer of Regulated CREB activity (TORC). This article reviews current knowledge on the mechanisms regulating CRH neuron activity. (C) 2011 Published by Elsevier Inc.
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