Animal models of CRH excess and CRH receptor deficiency display altered adaptations to stress.
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.
Coste
S C
SC
Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland, OR, USA.
Murray
S E
SE
Stenzel-Poore
M P
MP
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*
D018019:Receptors, Corticotropin-Releasing Hormone; D003346:Corticotropin-Releasing Hormone