Bartlett W P, Skoff R P
Department of Anatomy, Milton S. Hershey Medical Center, Hershey, PA 17033.
Brain Res Dev Brain Res. 1989 May 1;47(1):1-11. doi: 10.1016/0165-3806(89)90102-8.
The jimpy mutation is characterized by a severe deficiency of myelin formation throughout the central nervous system of hemizygous male mice. The female carrier of the jimpy gene is also hypomyelinated, but the myelin deficit in the female is less severe than age-matched controls, while the myelin content of 30-day-old carriers is nearly normal. Several different mechanisms might be employed by oligodendrocytes in the mosaic to compensate for the early myelin deficit. In the present autoradiographic study, we examine the ability of oligodendrocytes in the carrier to increase their rate of proliferation. Our results demonstrate that the number of oligodendrocytes incorporating tritiated-thymidine in the two-week mosaic is nearly 4 times greater than controls. The increased proliferation of oligodendrocytes is likely to be one mechanism which the mosaic utilizes to compensate for defective oligodendrocytes. The rate of glial proliferation returns to normal in older carriers. The rate of capillary cell proliferation was also significantly increased in the young mosaic, a phenomenon which does not occur in hemizygous males. These observations demonstrate the utility of the female carrier of the jimpy gene as a model to study the responses of glia and capillary cells to hypomyelination.