title: Animal models of CRH excess and CRH receptor deficiency display altered adaptations to stress.
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.
authors.affiliation: Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland, OR, USA.
authors.forename: S C
authors.initials: SC
authors.lastname: Coste
authors.forename: S E
authors.initials: SE
authors.lastname: Murray
authors.forename: M P
authors.initials: MP
authors.lastname: Stenzel-Poore
mesh_terms: D000818:Animals; D001519:Behavior / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena; D003346:Corticotropin-Releasing Hormone / Q000096:biosynthesis*; D004195:Disease Models, Animal; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D007107:Immune System / Q000503:physiopathology; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D010641:Phenotype; D018019:Receptors, Corticotropin-Releasing Hormone / Q000172:deficiency*; D013312:Stress, Physiological / Q000503:physiopathology*
chemical_list: D018019:Receptors, Corticotropin-Releasing Hormone; D003346:Corticotropin-Releasing Hormone