436 ZEMAN, CURTIS, SCARPELLI, AND KLEINFELD 



Fig. 5. U.U75 mm beam: 540, (JUO rad. 3U hours sur\i\al. Ctrcbellum. Capillary 

 with emerging compound granular cells. Frozen section. Holt's technique for esterases, 

 blocking with DFP, followed by siKer-carbonate impregnation. 



while in the lesions produced with 0.250 mm beams, the enzymes are pre- 

 dominately active within the interstitial cells. The degree of enzyme activity 

 is in direct proportion to the density of the nerve cell popidation. Thus, in 

 white matter, and to a lesser extent in the molecular layers, radiation-induced 

 activity of cathepsin-like enzymes is practically nil. 



The difference between the enzyme activity as elicited by beams of two 

 different sizes might be somehow related to dose rates. All lesions were pro- 

 duced with a high dose rate of 63,000 rad per sec. While such a dose rate 

 permits the enzymatic changes to develop with small beams, it appears to 

 introduce physico-chemical changes in the path of wider beams which hinder 

 the activation of cathepsin-like enzymes. Support for this assumption is 

 derived from previous studies in which one hemisphere of the mouse brain 



Fig. 6. 0.075 mm beam: 540,000 rad. 30 hours survival. Cerebellum. Note 2 Pur- 

 kinje cells with darkly staining cytoplasm. Some of the granule cells are similarly 

 affected, but this is difficult to appreciate on the photograph. Frozen section, Holt's 

 technique for esterases, blocking with DFP, followed by silver-carbonate impregnation. 



Fig. 7. 0.075 mm beam: 180,000 rad. 30 hours survival. Hippocampus. Cathepsin 

 activity in the cytoplasm of the granule cc41s. Holt's technique for esterases, blocking 

 with DFP, counter-stained with azocarmine. 



