Figure 7. TRPC1 overexpression activates the AKT/mTOR pathway in mice.

(A and B) SNpc regions were removed from control animals and animals overexpressing TRPC1 that had been treated or not with MPTP, and were subjected to SDS-PAGE and immunoblotting with the respective antibodies. Data are representative of 2–3 independent experiments. (C) Model for MPP⁺/MPTP-induced DA loss and TRPC1-mediated neuroprotection. MPP⁺/MPTP decreases the expression of TRPC1 and SOC-mediated Ca²⁺ influx either directly or indirectly via mitochondrial dysfunction. This leads to prolonged ER Ca²⁺ depletion and activation of the UPR and subsequent ER stress–mediated neurodegeneration. In contrast, TRPC1 overexpression restores SOCE function and maintains ER Ca²⁺ homeostasis. Further, Ca²⁺ influx through TRPC1 activates AKT/mTOR-mediated survival mechanisms in DA cells, which leads to increased neuronal survival.