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.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
-
Review
MeSH terms
-
Animals
-
Behavior / physiology
-
Cardiovascular Physiological Phenomena
-
Corticotropin-Releasing Hormone / biosynthesis*
-
Disease Models, Animal
-
Hypothalamo-Hypophyseal System / physiopathology*
-
Immune System / physiopathology
-
Mice
-
Mice, Knockout
-
Mice, Transgenic
-
Phenotype
-
Receptors, Corticotropin-Releasing Hormone / deficiency*
-
Stress, Physiological / physiopathology*
Substances
-
Receptors, Corticotropin-Releasing Hormone
-
Corticotropin-Releasing Hormone