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Fig. 2 | Molecular Brain

Fig. 2

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

Fig. 2

MtCB1 regulated metabolic defects following TBI. Traumatic injury changed metabolite levels in wild types, CB−/− mouse brains as well as neuronal models (A1–A4, B1–B4 and D1–D4). THC and AM251 reversely mediated metabolite levels in wild type mice brain following TBI (A1–A4). THC and AM251 did not affect metabolite levels in CB−/− mice brain following TBI (B1–B4). Hemopressin did not affect metabolite levels in wild type mice brain following TBI (C1–C4). Traumatic injury changed metabolite levels in cultured neuronal models (D1–D4). HU210 and AM251 reversely mediated metabolite levels in cultured neurons following injury (D1–D4). HU210 and AM251 did not changed metabolite levels in cultured CB−/− neurons following injury (E1–E4). HU210-biotin and hemopressin did not affect metabolite levels in cultured neurons (F1–F4). HU210 and AM251 reversely mediated metabolite levels in mitochondria separated from cultured neurons or wild-type mice after injury, but not in mitochondria from CB1−/− mice after injury (G1-G4). Data were expressed as mean ± SE (**p < 0.01 versus sham, ***p < 0.001 versus sham, #p < 0.05 versus vehicle, ##p < 0.01 versus vehicle, ###p < 0.001 versus vehicle)

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