20 ROBERTS RUGH 



that fetal irradiation of the rat results in a neurologically deficient embryo: 

 "The cerebral hemispheres and diencephalon were a a^ood deal smaller 

 than normal. . . . The neocortex was seriously deficient, and about half as 

 thick as normal at the vertex to about 2^ normal thickness laterally. . . . 

 Small pallium. . . . The anterior commissure was a little less compact. . . . 

 The midbrain was smaller in total cross area than normal due to somewhat 

 flattened superior colliculi. . . . The cerebellum was altosjether a little 

 smaller than normal. . . . The lower medulla showed a slight reduction 

 in total o\er-all size. . . . The lower brain stem and cerebellum were a little 

 smaller than normal. . . . The cords were a little smaller in cross section 

 than normal. . . . Most of the cells in the 13-day retina were killed by 

 radiation." 



Anomalies mentioned in this excellent study included: 



"Radiation-killed cells in the periependymal primitive matrix threw the 

 mitotic layer into rosettes which continued to proliferate brain, nonetheless. 

 The result was an anomalous mass of ectopic cortex. . . . No corpus cal- 

 losum. . . . Bizarre bundles of fibers. . . . Disorderly array of all sorts of 

 cortical neurons. . . . The neurons were jumbled, scattered, and they were 

 often upside down or pointed sideways." 



Figs. 28-35 are on pages 18 and 19. 



Figs. 28, 29, and 30. These represent members of litters from 3 successive genera- 

 tions following a single exposure of the ovary of the mother of those in Fig. 28 to 

 100 r. It was whole-body e.xposure, but we have reason to believe that the somatic 

 eflFects of this exposure had nothing to do with these congenital anomalies. The fact 

 that a single exposure of the ovary caused this brain anomaly to appear in three suc- 

 cessive generations is genetically significant, even though its incidence was very low. 



Fig. 31. These represent an entire litter from a grandfather who had received high- 

 level exposure of his testis. The first generation appeared normal, were viable and 

 fertile. This brain anomaly of exencephalia appeared in the next generation. One 

 might expect it to appear in yet succeeding generations. 



Fig. 32. The four embryos to the right show the variety of anomalies which ap- 

 peared in the second generation following testis exposure. All were stunted, some died 

 as fetuses (late in development). The single member to the left is a control of the 

 same age. 



Fig. 33. When mouse embryos are exposed after organogenesis to high but tolerable 

 levels of irradiation, the eflFects are largely skeletal. Note particularly the variations in 

 size within the single litter. One member of the litter is almost as large as the controls. 

 The explanation of this is probably genetic. 



Fig. 34. This is one litter, all of whom were exposed at the same time to the same 

 irradiation, but which exhibit a wide range of difference in size. 



Fig. 35. This shows photographs of Spalteholz's preparations of two mice at birth, 

 the upper one being the control, the lower one x-irradiated at 13.5 days. Note that 

 the irradiated embryo appears to be topograhically normal but obviously is very much 

 stunted. The developmental processes have been able to reorganize the undamaged 

 cells to provide an apparently normally proportioned but stunted mouse. 



