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Fig. 4 | Molecular Brain

Fig. 4

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

Fig. 4

MtCB1 regulated neuronal metabolic defects and apoptosis through mitochondrial cAMP/PKA/complex I pathway. HU-210 inhibited cAMP/PKA/complex I activity in mitochondria purified from injured neurons and wild type mice while AM251 showed opposite effect (A1, B1). Mitochondrial cAMP/PKA/complex I pathway inhibitor H89 or rotenone promoted mitochondrial metabolic defects, cyt c and AIF release (A2, A3, B2 and B3) while the activator forskolin showed opposite effects (A4 and B4). HU210 and AM251 did not affect cAMP/PKA/complex I activity in mitochondria purified from CB−/− mice following injury (c). Tom20 is a mitochondrial protein. Data were expressed as mean ± SE. (#p < 0.05 versus vehicle, ##p < 0.01 versus vehicle)

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