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. 2004 Jan 2;101(2):665–670. doi: 10.1073/pnas.0307453101

Fig. 3.

Fig. 3.

Comparison of MPTP-induced nigrostriatal pathway injury in WT and Jnk–/– mice. (A) Peroxidase immunohistochemistry for TH on midbrain sections from saline- and MPTP-injected WT and JNK-deficient mice. (Scale bar represents 200 μm.) (B) Stereological counts of TH-positive cells in the SNpc at 7 days after MPTP intoxication. JNK2 or JNK3 ablation elicits sparing of TH-positive neurons after MPTP treatment, as compared with WT mice. Dual deletion of JNK2 and JNK3 increases the protective effect further. *, P < 0.01, compared with MPTP-injected WT mice (Mann–Whitney U test). (C and D) Motor performance of saline- or MPTP-treated WT and JNK-deficient mice measured on a Rotarod. The mean times on the rod recorded for increasing rod-rotation speeds (8–15 mice per group; C) and the mean overall rod performance (ORP, see Materials and Methods) for each group of mice (D) show that MPTP-intoxicated JNK-deficient animals display significant improvement of motor functions compared with MPTP-treated WT mice. *, P < 0.05, by Mann–Whitney U test.