RADIATION AND AUDIOGENIC SEIZURES IN MICE 527 



ground level fluctuated, but remained high, reaching a peak from October, 

 1958, through April, 1959, then gradually declining. Table VIII shows the 

 percentage of fatal seizures on the 1st trial in 3 groups of untreated mice (Fi, 

 backcross, and DBA/1) during 9 intervals of several months each. The 

 figures extend through the 27 months during which the background level 

 was changing. A "relative fallout" figure is shown for each time interval, 

 based on fallout records supplied by Health Physics, the Atomic Energy 

 Commission, and Argonne National Laboratory. 



The 3 populations of control mice responded differently to the changing 

 background level. The Fi group, with intermediate seizure susceptibility, 

 shows the closest correlation with fallout le\el. In the backcross generation, 

 a low susceptibility group, the response did not change significantly until the 

 second increase in background, after which the incidence of fatalities in- 

 creased. The DBA/1 mice, the most seizure prone, appear to have a low 

 threshold for radiation efTect. The incidence of fatalities was stimulated 

 maximally at the first rise in fallout and showed little further change until 

 the extreme decline in background level late in 1959. Some lag in the effect 

 of fallout rate was obser\ed; this would be expected on the basis of the 

 contribution of fallout to food content and to dust in the animal rooms. 

 (The lower incidence of fatalities during May to September, 1958 almost 

 certainly is related to lower background in the mouse quarters despite the 

 high fallout rate. At that time the whole installation was thoroughly scrubbed 

 and disinfected because of an infestation of mites.) 



It should be emphasized that the changes in seizure frequency were ob- 

 served first, and the figures on fallout were obtained later in an eflFort to 

 explain the shifts in our data. 



A series of DBA/2 mice, maintained in Room G at background, were 

 injected with 20 mg glutamic acid between June, 1959, and February. 1960. 

 The protective eflfect of glutamate on the incidence of seizures was moderate, 

 with a slight reduction in total incidence, but a higher proportion of non- 

 fatal seizures. However, the curve representing the latency of fatal seizures 

 in this group was unlike that obtained in Room G during the earlier period 

 of low background (Fig. 3). Figure 4 shows the latency curves of DBA/2 

 control mice and those injected with glutamate. For comparison, we have 

 added the curve showing the latency of glutamate-injected mice maintained 

 in Room R under chronic low level gamma radiation during 1954. In the 

 uninjected controls, the early peak was exaggerated over the typical DBA/2 

 curve, with an unusual proportion of the mice convulsing between 6 and 10 

 sec after the onset of stimulation. In the mice injected with glutamate the 

 latency figures were similar to those of the earlier group reared in Room R • 

 the difference shown in the high background group is in the direction of 

 shorter latency, indicating greater seizure susceptibility. These cur\ es suggest 



