Figures & data
Figure 1. Increased calcium level in the lumbar motor neurons of mutant SOD1 Tg mice. An increased number of electron-dense deposits (EDDs; arrows) is noted, reflecting the distribution of calcium in the motor neurons in the talampanel-treated (A) and the vehicle-treated (B) mutant SOD1 Tg mice at the age of 19 weeks. Motor neurons from the wild-type mice at the same age contain fewer deposits, regardless of whether they were treated with talampanel (C) or with vehicle only (D). Besides the increased number of EDDs in the mutant SOD1 Tg animals, mitochondrial degeneration with clusters of EDDs (asterisk) was frequently seen. In the wild-type animals, regardless of the treatment, no structural alterations were present. Mit: mitochondrion, Go: Golgi complex. Bar: 500 nm.
Figure 2. Effects of talampanel treatment on the calcium level of lumbar motor neurons of mutant SOD1 Tg mice. The volume occupied by electron-dense deposits (EDDs), reflecting tissue calcium, relative to the perikaryal volume was determined in mutant SOD1 Tg (mSOD1-Tg) and wild-type (wt) animals after talampanel (Ta) or vehicle (Ve) treatment at 12 (A) and 19 (B) weeks of age. Talampanel had a significant effect in reducing the calcium level only at the age of 12 weeks (asterisk; p = 0.01, two-way ANOVA with Duncan post hoc comparison). Data are shown as means ± SEM.
Figure 3. Effects of talampanel treatment on the number of lumbar motor neurons in mutant SOD1 Tg mice. Relative to the vehicle-only treatment (Ve), talampanel treatment (Ta) did not exert a significant effect either in the mutant SOD1 Tg (mSOD1-Tg), or in the wild-type (wt) mice in the presymptomatic (A) or a later stage of the disease (B). Regardless of the treatment, lower cell numbers were counted at 19 weeks of age than at 12 weeks of age in the mutant SOD1 Tg animals. Data are shown as means ± SEM.
