4.4 Article

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

Journal

PEPTIDES
Volume 22, Issue 5, Pages 733-741

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/S0196-9781(01)00386-2

Keywords

allostasis; corticotropin-releasing hormone; knock-out mice; stress; transgenic; urocortin

Funding

  1. NHLBI NIH HHS [HL55512] Funding Source: Medline
  2. NIAAA NIH HHS [P60 AA010760] Funding Source: Medline
  3. NIAID NIH HHS [T32 AI07472] Funding Source: Medline
  4. NIMH NIH HHS [MH55722] Funding Source: Medline

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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-R 1) 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. (C) 2001 Elsevier science Inc. All rights reserved.

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