| First Author | Grant FD | Year | 2000 |
| Journal | Exp Physiol | Volume | 85 Spec No |
| Pages | 203S-209S | PubMed ID | 10795924 |
| Mgi Jnum | J:62451 | Mgi Id | MGI:1858890 |
| Doi | 10.1111/j.1469-445x.2000.tb00025.x | Citation | Grant FD (2000) Genetic models of vasopressin deficiency. Exp Physiol 85 Spec No:203S-209S |
| abstractText | Animal models of genetic hormone deficiency are useful as models for physiological studies of hormone deficiency and hormone action. Structure-function studies of the specific underlying gene defect may help in understanding mechanisms regulating gene expression and secretion of the peptide product. Spontaneous genetic models of vasopressin deficiency, such as the Brattleboro rat and human familial diabetes insipidus, have facilitated many studies of vasopressin. However, the Brattleboro rat may not be an ideal model of genetic vasopressin deficiency and therefore could be less useful for studies of the central nervous system or as a background strain for the introduction of new vasopressin gene constructs. The human model is appropriately limited by the constraints of human studies, so that engineered animal models of specific diseases, such as familial neurohypophysial diabetes insipidus, are required. The recent development of a vasopressin-null mouse may provide insights into the various roles of vasopressin in the stress response, cardiovascular regulation and behaviour. Additionally, animals with a complete genetic deficiency of vasopressin can serve as a background strain for introduction of novel vasopressin gene constructs to enable sophisticated studies of the regulation of vasopressin expression and the intracellular processes required for appropriate secretion of vasopressin peptide. As advanced techniques of genetic manipulation become more reliable, conditional expression of vasopressin, regulated by time or body site will permit even more detailed studies in this field. |
