The Mitochondrial Toxin 3-Nitropropionic Acid Induces Striatal Neurodegeneration via a c-Jun N-Terminal Kinase/c-Jun Module

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Fig. 4.
Fig. 4.

Systemic administration of 3-NP leads to a progressive activation of JNK in the striatum selectively. JNK activation was analyzed by immunocytochemical detection of its active, phosphorylated form (P-JNK) from sections corresponding to the rats used for behavioral, histological, and TUNEL analysis (see previous figures). A, High magnification of P-JNK immunoreactivity in the piriform cortex and DM and DL regions of the striatum. Note the lack of labeling in the Piriform cortex and the DM striatum inControl and 3-NP-treated rats. P-JNK immunoreactivity appears at 3-NP-5 days in theDL striatum specifically. B, P-JNK-immunoreactive cells were depicted in the striatum using an image analyzer. Note their appearance in the DL striatum specifically at 3-NP-5 days treatment. C, Quantification of P-JNK-immunoreactive cells was performed from at least five different rats per neurological score. For each rat, one equivalent striatal section (30 μm) was counted. Shown is the mean value determined in 3-NP-treated rats presenting the same neurological score. <5, Three to 4 d of 3-NP treatment;5–6, 5 d of treatment; 7–8, 6 d of treatment. Statistical analysis: *p < 0.005 when comparing scores 7–8 and <5(Scheffé test).

  1. The Journal of Neuroscience vol. 22 no. 6 2174-2184
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