| First Author | Dung HC | Year | 1975 |
| Journal | Anat Rec | Volume | 181 |
| Pages | 347-348 (Abstr.) | Mgi Jnum | J:12166 |
| Mgi Id | MGI:60416 | Citation | Dung HC (1975) Growth retardation, high mortality, and low reproductivity of neurological mutant mice. Anat Rec 181:347-348 (Abstr.) |
| abstractText | Full text of Abstract: DUNG, H.C., Department of Anatomy, The University of Texas Health Science Center at San Antonio, San Antonio, Texas. Growth retardation, high mortality rate. and low reproductivity of neurological mutant mice. Neurological mutant mice are characterized by their abnormal behavior. Attempts to establish pathological lesions in the central nervous system of a number of the affected animals namely tumbler, torpid, lethargic, dancer, fidget, pivot and pirouette, failed to show significant difference from that of normal animals. It is possible that the primary action of these various mutant genes is not on the central nervous system. Instead, judging from the experimental data obtained, it is theorized that the mutant gene affects primarily endocrine glands and lymphoid organs, as indicated by the common clinical symptoms of the growth retardation, high mortality rate, and low reproductivity among various mutant mice. In three neurological mutants of the mouse studied, tumbler, torpid, and lethargic, it was observed by light microscope that their pituitary glands showed indications of pathological changes. There appeared to be an increase in the cellular population density due to the scanty amount of cytoplasm in the pituitary cells. The pituitary of torpid female mice was studied by electron microscope. It was seen that the prolactin cells were remarkably deficient. In normal siblings this cell type constituted 40% of the entire cell population whereas in torpid mice it was only 10%. Such deficiency in the pituitary may account for the growth retardation and low reproductivity of the mutants. Another cause of low reproductivity may lie in ovarian dysfunction; ovaries of the mutant mice were invariably found to contain no corpora lutea and the interstitial cells were dystrophic. The cause of a high mortality rate among affected mice between the third and fourth week after birth is likely due to an alteration in the immunological status of the mutants. Lymphoid tissues of tumbler, torpid, and lethargic mice were studied. The thymus was found to undergo involution soon after the onset of neurological symptoms. Immunological deficiency was also indicated by other studies. (Supported by a grant of Morrison Trust Foundation and an Institutional Research Grant of The University of Texas Health Science Center at San Antonio.) |
