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Hypothalamic-pituitary-adrenal axis disregulation in PrPC-null mice
Manuel Sanchez-Alavez1, José R Criado, Izabella Klein
1Molecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, California 92037, USA.
Neuroreport
|September 18, 2008
Summary
The cellular prion protein (PrPC) influences the stress response. PrPC-deficient mice exhibit impaired negative feedback in the hypothalamic-pituitary-adrenal axis, suggesting PrPC
Area of Science:
- Neuroendocrinology
- Prion Biology
Background:
- Prion diseases affect hypothalamic and pituitary functions.
- The role of cellular prion protein (PrPC) in neuroendocrine regulation is unclear.
Purpose of the Study:
- To investigate the role of PrPC in modulating the hypothalamic-pituitary-adrenal (HPA) axis.
- To compare HPA axis activity in PrPC-deficient (PrP 0/0) and wild-type (PrP+/+) mice.
Main Methods:
- Measurement of corticosterone and adrenocorticotropic hormone (ACTH) levels.
- Comparison of HPA axis response to acute stress in PrP 0/0 and PrP+/+ mice.
- Assessment of the effect of corticosterone and dexamethasone on ACTH levels post-stress.
Main Results:
- PrP 0/0 mice displayed hypercorticism during the dark cycle.
- Both mouse types showed similar initial increases in corticosterone and ACTH after stress.
- ACTH remained elevated in PrP 0/0 mice post-stress, despite high corticosterone levels.
- Corticosterone and dexamethasone inhibited stress-induced ACTH elevation in PrP+/+ mice, but not in PrP 0/0 mice.
Conclusions:
- PrPC is implicated in the negative feedback regulation of the HPA axis.
- PrPC deficiency disrupts the normal inhibitory control of corticosterone on ACTH release.
- These findings highlight a novel function of PrPC in maintaining HPA axis homeostasis.
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