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Hypothalamic-pituitary-adrenal axis disregulation in PrPC-null mice

Academic Article
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Overview

authors

  • Sanchez-Alavez, Manuel
  • Criado, J. R.
  • Klein, I.
  • Moroncini, G.
  • Conti, Bruno

publication date

  • October 2008

journal

  • Neuroreport  Journal

abstract

  • As manifestations of prion diseases include disturbances of hypothalamic and pituitary functions, we tested the hypothesis that the cellular prion protein (PrPC) has a role as modulator of the hypothalamic-pituitary-adrenal axis. The level of corticosterone and adrenocorticotropic hormone were compared in PrPC null (PrP 0/0) and wild-type (PrP+/+) mice. PrP 0/0 showed hypercorticism during the dark part of day. After acute stress, corticosterone and adrenocorticotropic hormone increased similarly in PrP+/+ and PrP 0/0 mice. Adrenocorticotropic hormone, however, remained elevated in PrP+/+ 0/0 mice at corticosterone levels that are inhibitory in PrP mice. Pretreatment with corticosterone or dexamethasone inhibited stress-induced elevation of adrenocorticotropic hormone in PrP+/+ but not in PrP 0/0 mice. Thus, PrPC may play a role in the negative feedback regulation of axis.

subject areas

  • Adrenocorticotropic Hormone
  • Animals
  • Corticosterone
  • Dexamethasone
  • Genotype
  • Glucocorticoids
  • Hypothalamo-Hypophyseal System
  • Mice
  • Mice, Knockout
  • Pituitary-Adrenal System
  • PrPC Proteins
  • Radioimmunoassay
  • Restraint, Physical
  • Stress, Psychological
  • Time Factors
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Research

keywords

  • adrenal
  • adrenocorticotropic hormone
  • corticosteroid
  • hypothalamic-pituitary-adrenal
  • hypothalamus
  • prion
  • stress
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Identity

PubMed Central ID

  • PMC2649708

International Standard Serial Number (ISSN)

  • 0959-4965

Digital Object Identifier (DOI)

  • 10.1097/WNR.0b013e32830fle90

PubMed ID

  • 18797300
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Additional Document Info

start page

  • 1473

end page

  • 1477

volume

  • 19

issue

  • 15

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