Animal models of CRH excess and CRH receptor deficiency display altered adaptations to stress

Sarah C. Coste, Susan E. Murray, Mary P. Stenzel-Poore

Research output: Contribution to journalArticle

100 Scopus citations

Abstract

This review highlights new information gained from studies using recently developed animal models that harbor specific alterations in corticotropin-releasing hormone (CRH) pathways. We discuss features of a transgenic mouse model of chronic CRH overexpression and two mouse models that lack either CRH receptor type 1 (CRH-R1) or type 2 (CRH-R2). Together these models provide new insights into the role of CRH pathways in promoting stability through adaptive changes, a process known as allostasis.

Original languageEnglish (US)
Pages (from-to)733-741
Number of pages9
JournalPeptides
Volume22
Issue number5
DOIs
StatePublished - May 14 2001

Keywords

  • Allostasis
  • Corticotropin-releasing hormone
  • Knock-out mice
  • Stress
  • Transgenic
  • Urocortin

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Endocrinology
  • Cellular and Molecular Neuroscience

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