Antidyskinetic Treatment with MTEP Affects Multiple Molecular Pathways in the Parkinsonian Striatum

Figure 4

(a–c) Protein levels were evaluated by western blotting of samples from the lesioned side of the striatum (% of PD). (a) Protein level of PKC expressed relative to the level of β-actin in the 6-OHDA-lesioned rats treated with saline, L-Dopa (25 mg/kg) plus benserazide (6.25/kg), and MTEP. (b) Protein level of p-MEK level expressed relative to the total MEK level in the 6-OHDA-lesioned rats treated with saline, L-Dopa (25 mg/kg) plus benserazide (6.25/kg), and MTEP expressed relative to the level of β-actin in the sample. (c) p-ERK1/2 level expressed relative to the total ERK1/2 level in the 6-OHDA-lesioned rats treated with vehicle, L-Dopa (25 mg/kg) plus benserazide (6.25/kg), and MTEP expressed relative to the level of β-actin in the sample. Comparisons with the LID group revealed that MTEP prevented the increase of PKC, p-MEK, and p-ERK1/2 after chronic L-Dopa treatment ). Comparisons with the PD group revealed that PKC, p-MEK, and p-ERK levels were increased in the LID group, but there is a minor decrease in the PKC and MEK expression level (); there is no significant difference in the p-ERK1/2 expression level. The data represent the mean relative optical density ± SD (one-way ANOVA, per group).

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