| First Author | Venihaki M | Year | 1999 |
| Journal | Front Neuroendocrinol | Volume | 20 |
| Issue | 2 | Pages | 122-45 |
| PubMed ID | 10328987 | Mgi Jnum | J:55288 |
| Mgi Id | MGI:1337581 | Doi | 10.1006/frne.1999.0179 |
| Citation | Venihaki M, et al. (1999) Animal models of CRH deficiency. Front Neuroendocrinol 20(2):122-45 |
| abstractText | Corticotropin-releasing hormone (CRH), the major regulator of hypothalamic-pituitary-adrenal (HPA) axis, was first isolated due to its ability to stimulate the release of adrenocorticotropic hormone from the anterior pituitary. Later, it was also found to have also a wide spectrum of actions within the central nervous system and the periphery. Studies with pharmacological administration of this peptide and/or antagonists and antibody neutralization techniques have yielded important information concerning the physiological relevance of CRH. The development of CRH knockout mice (CRH KO) has been an important tool for addressing the physiologic and pathologic roles of CRH. This review describes the phenotype of CRH-deficient mice, as well as the use of this model to study the roles of CRH on fetal development and postnatal life. The role of CRH in prenatal development and postnatal regulation of the HPA axis, in activation of the reproductive system during stress, and in modulation of the immune function will be discussed. The review concludes with a comparison of CRH KO mice with other models of CRH deficiency. Copyright 1999 Academic Press. |
