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

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

Research output: Contribution to journalArticle

99 Citations (Scopus)

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 - 2001

Fingerprint

Corticotropin-Releasing Hormone Receptors
Corticotropin-Releasing Hormone
Animals
Animal Models
Display devices
Allostasis
Transgenic Mice
Ports and harbors

Keywords

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

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology
  • Cellular and Molecular Neuroscience

Cite this

Animal models of CRH excess and CRH receptor deficiency display altered adaptations to stress. / Coste, Sarah C.; Murray, Susan; Stenzel-Poore, Mary.

In: Peptides, Vol. 22, No. 5, 2001, p. 733-741.

Research output: Contribution to journalArticle

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