@entity3147 in infancy as a susceptibility factor for temporal lobe epilepsy in adulthood induced by the XXXX experimental model.

@entity410 @entity16 @entity28802 @entity2134 @entity302 @entity3147 @entity35 @entity159
@entity3147 during the earliest stages of life may result in innumerable brain problems. Moreover, this condition could increase the chances of developing @entity16 , such as @entity302 . We analyzed the effects of early-life @entity3147 on susceptibility to @entity302 induced by the @entity2134 model of @entity302 . @entity35 @entity35 pups were kept on a starvation regimen from day 1 to day 21 after birth. At day 60, 16 animals (8 = well-nourished; 8 = malnourished) were exposed to the @entity2134 experimental model of @entity302 . Age-matched well-nourished (n = 8) and malnourished (n = 8) @entity35 were used as controls. Animals were video-monitored over 9 weeks. The following behavioral parameters were evaluated: first @entity410 threshold (acute period of the @entity2134 model); @entity159 ( @entity159 ) latency; first spontaneous @entity410 latency (silent period), and spontaneous @entity410 frequency during the chronic phase. The cell and @entity28802 ( @entity28802 ) density were evaluated in the hippocampal formation. Our results showed that the malnourished animals required a lower @entity2134 dose in order to develop @entity159 (200 mg/kg), lower latency to reach @entity159 , less time for the first spontaneous @entity410 and higher @entity410 frequency, when compared to well-nourished @entity2134 @entity35 . Histopathological findings revealed a significant cell density reduction in the CA1 region and intense @entity28802 among the malnourished animals. Our data indicate that early @entity3147 greatly influences susceptibility to @entity410 and behavioral manifestations in adult life. These findings suggest that @entity3147 in infancy reduces the threshold for @entity302 and promotes alterations in the brain that persist into adult life.
