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Fig. 5 | Molecular Brain

Fig. 5

From: Acute upregulation of neuronal mitochondrial type-1 cannabinoid receptor and it’s role in metabolic defects and neuronal apoptosis after TBI

Fig. 5

TBI induced AKT accumulation in neuronal mitochondria and mtCB1 regulated mitochondrial AKT/complex V activity. Western blot analysis of mitochondrial total AKT and pAKT showed AKT greatly increased in mitochondria separated from neurons, wild type or CB1−/− mice 24 h post injury and most of them are unphosphorylated (A1 and A2). HU210 increased AKT/complex V activity in mitochondria purified from cultured neurons or wild type mice while AM251 showed opposite effects (A3 and A4). HU-210 and AM251 did not affect AKT/complex V activity in mitochondria from CB1−/− mice (b). Tom20 is a mitochondrial protein. Data were expressed as mean ± SE. (##p < 0.01 versus vehicle, *p < 0.05 versus sham, ***p < 0.001 versus sham)

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