Fig. 7 | Cellular and Molecular Life Sciences

Fig. 7

From: Bafilomycin A1 activates respiration of neuronal cells via uncoupling associated with flickering depolarization of mitochondria

Fig. 7

Baf increases susceptibility of dPC12 to excitatory stimulation. a Pretreatment with 0.25 μM Baf dramatically increases the respiratory response to ΔΨp depolarization by high K+. The response is not reduced by the SERCA inhibitor thapsigargin. The dashed line shows the level of deoxygenation induced by K+ in the Baf(−) cells treated with thapsigargin. b In Ca2+-free medium Baf(+) cells do not respond to high K+ and rapidly loose their respiratory activity. c Pretreatment with Baf (25 μM, 30 min) in glucose(+) medium reduces elevation of ATP in response to ΔΨp depolarization by high K+, whereas in galactose(+) medium K+ stimulation strongly decreases cellular ATP. The effect of CMA (0.25 μM) on the ATP response to K+ is less pronounced. Valinomycin (Val, 0.25 μM) in galactose(+) conditions reduces the ATP by >90%, irrespective of K+ treatment. d Pretreatment of the cells with 25 μM Baf for 30 min amplifies the dose-dependent response to glutamate (5–20 mM), while CMA does not affect the response to glutamate. e Relative decrease in cellular ATP (measured 20 h after glutamate treatment) reveals a negative effect of Baf on the viability of dPC12 cells, exposed to glutamate. DMSO was used as a negative control. Asterisks significant differences

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