Journal
TRENDS IN NEUROENDOCRINOLOGY
Volume 1220, Issue -, Pages 49-59Publisher
BLACKWELL SCIENCE PUBL
DOI: 10.1111/j.1749-6632.2011.05904.x
Keywords
stress response; neuropeptides; PACAP; HPA axis; hypothalamus
Funding
- NIMH-IRP [Z01-MH002386-21, Z01-MH002386-22, Z01-MH002386-23, Z01-MH002386-24]
- NATIONAL INSTITUTE OF MENTAL HEALTH [ZIAMH002386, Z01MH002386] Funding Source: NIH RePORTER
Ask authors/readers for more resources
The neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) is released from stress-transducing neurons. It exerts postsynaptic effects required to complete the hypothalamo-pituitary-adrenocortical (HPA) and hypothalamo sympatho adrenal (HSA) circuits activated by psychogenic and metabolic stressors. Upon activation of these circuits, PACAP-responsive (in cell culture models) and PACAP-dependent (in vivo) transcriptomic responses in the adrenal gland, hypothalamus, and pituitary have been identified. Gene products produced in response circuits during stress include additional neuropeptides, neurotransmitter biosynthetic enzymes, and neuroprotective factors. Major portions of HPA and HSA stress responses are abolished in PACAP-deficient mice. This deficit occurs at the level of both the hypothalamus (HPA axis) and the adrenal medulla (HSA axis). PACAP-dependent transcriptional stress responses are conveyed through noncanonical cyclic AMP- and calcium-initiated signaling pathways within the FISA circuit. PACAP transcriptional regulation of the HPA axis, in the hypothalamus, is likely to be mediated via canonical cyclic AMP signaling through protein kinase A.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available