RADIATION AND AUDIOGENIC SEIZURES IN MICE 523 



quency of total and fatal seizures was significantly greater among the Room 

 R litters than in the Room G controls. At this time, a series of backcross 

 litters were irradiated at Argonne Hospital, receiving 1.5-2 r between days 

 23 and 30. While the incidence of seizures was close to that observed in 

 Room R, the elevation was greater in females than in males. Another 

 unexpected control period occurred in 1958 when the source was not in 

 use, followed by a period of exposure to 0.2 mr per hour. 



The higher frequency of seizures among the controls in Room G begin- 

 ning in September, 1957, coincided with increasingly high background from 

 radioactive fallout (to be discussed below.) The data summarized in Table 

 V lend further support to the belief that the radiation level in Room R was 

 responsible for the elevation of the incidence of audiogenic seizures among 

 the mice reared in this environment. 



Glutamate Protection in DBA/2 



In DBA/2 mice, the incidence of audiogenic seizures is so high, approach- 

 ing 100%, that any increase in susceptibility would ordinarily not be detect- 

 able. However, in a series of mice injected with glutamic acid, we have 

 evidence that low level radiation also influences the sound susceptibility of 

 these mice. Glutamic acid, injected as monosodium glutamate 30-45 minutes 

 before the sound test, gives almost complete protection from seizures in 

 DBA/1. 



In 1954, Dr. Benson Ginsburg at Jackson Laboratory, found that one 

 injection of glutamic acid (20 mg per 10 g body weight) confers significant 

 protection from audiogenic seizures in DBA/2 mice, with the seizure fre- 

 quency reduced more in females than in males. In the same summer, we 

 attempted to enlarge his series, using the same dosage in our DBA/2 line. 

 These mice, derived from Jackson Laboratoiy stock, had been maintained 

 by brother-sister matings in our laboratory since 1951. Twenty mg of glu- 

 tamic acid gave little, if any, protection from seizures in mice kept in Room 

 R (Table VI). With 30 mg, protection was only moderate. In 1957, with 

 the mice maintained in Room G at background, the glutamic acid series was 

 repeated, using DBA/2 mice which were direct descendants of those in the 

 1954 series. In the absence of radiation, 20 mg glutamic acid reduces signifi- 

 cantly the frequency of seizures and deaths; at 30 mg, the protection is ex- 

 cellent. Contraiy to Ginsburg's findings, however, we observed no sex dif- 

 ference in the response to glutamic acid, possibly an indication of genetic 

 change in our DBA/2 line. 



Additional evidence of a diflference in response to glutamic acid in the 

 presence and absence of low level radiation is seen in the latency of fatal 

 seizures during the two periods. Figure 3 shows the latency curves of control 



