促肾上腺皮质激素释放激素（CRH）过量和CRH受体缺乏的动物模型表现出对压力的适应性改变。
Animal models of CRH excess and CRH receptor deficiency display altered adaptations to stress.
作者信息
Coste S C, Murray S E, Stenzel-Poore M P
机构信息
Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland, OR, USA.
出版信息
Peptides. 2001 May;22(5):733-41. doi: 10.1016/s0196-9781(01)00386-2.
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.
本综述重点介绍了利用最近开发的动物模型所获得的新信息，这些模型在促肾上腺皮质激素释放激素（CRH）途径中存在特定改变。我们讨论了慢性CRH过表达转基因小鼠模型以及缺乏1型CRH受体（CRH-R1）或2型CRH受体（CRH-R2）的两种小鼠模型的特点。这些模型共同为CRH途径在通过适应性变化促进稳定性（这一过程称为同态调节）中的作用提供了新的见解。
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