Diacylglycerol Signaling Underlies Astrocytic ATP Release

Figure 5

OAG-induced ATP release from astrocytes appears to be vesicular. (a) Incubation of cultured astrocytes with 100 nM Bafilomycin A1, an inhibitor of the vesicular H⁺  ATPases that set up the proton gradients necessary for vesicle filling, greatly reduced OAG-induced astrocytic ATP release (bafilomycin 𝑛=8, control 𝑛=5;𝑡1𝑃=0.01,𝑡2𝑃=0.02,𝑡3𝑛=0.004). This effect was partially washed out after 15 minutes (𝑡2 bafilomycin versus 𝑡3 wash 𝑃=0.024). (b) Bafilomycin treatment did not affect the function of astrocytic ATP receptors, as the calcium response to 1 μM ATP was unaffected by bafilomycin treatment (bafilomycin 𝑛=5, control 𝑛=5,𝑃=0.9). (c) The gap junction and hemichannel blocker carbenoxolone (CBX), at 50 μM, resulted in an increase in astrocytic ATP release (control 𝑛=14, CBX 𝑛=5;𝑡2𝑃=0.03,𝑡3𝑃=0.02).

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(b)

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