Format

Send to

Choose Destination
Front Neuroendocrinol. 2012 Jan;33(1):67-84. doi: 10.1016/j.yfrne.2011.08.002. Epub 2011 Aug 18.

The molecular physiology of CRH neurons.

Author information

1
Section on Endocrine Physiology, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shiver Institute of Child Health and Human Development, NIH, Bethesda, MD 20892, United States. Greti_Aguilera@nih.gov

Abstract

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.

PMID:
21871477
PMCID:
PMC4341841
DOI:
10.1016/j.yfrne.2011.08.002
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center