Fig. 3. Schematic representation of pKr-2-mediated neurotoxicity in the SN. Breakdown of the blood-brain barrier may be involved in an influx of prothrombin, which consequently resulting in the production of thrombin and pKr-2 in the SN. The increased pKr-2 may be translocated within microglia, and microglial activation may be mediated by the induction of microglial TLR4 following pKr-2 translocation. Activated microglia can produce neurotoxic cytokines and reactive oxygen species (ROS). These neurotoxic factors induce dopaminergic (DA) neuronal death.
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