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. 2015 Aug 4;6:7844. doi: 10.1038/ncomms8844

Figure 4. Ca2+ increase in OPC processes is mediated by glutamate and ATP released in response to action potentials in axons.

Figure 4

(a) Representative Ca2+ traces in OPC processes in response to electrical stimulation of axons without (black) and with (blue) BoNT/A treatment to block SNARE-dependent exocytosis. (b) Averaged Ca2+ traces in OPCs from 14 dishes are shown. Responses were inhibited by BoNT/A treatment. **P=0.001, t-test, peak amplitude, n=14 cells from 14 dishes with no BoNT/A, n=14 cells from 14 dishes with BoNT/A. (c) Number of Ca2+ responses were reduced significantly by BoNT/A treatment (blocked). The peak Ca2+ response within 200 s of axonal stimulation (10 Hz) were measured. P=0.004, t-test, n=14 cells from 14 dishes with no BoNT/A, n=14 cells from 14 dishes with BoNT/A. (d) Summary graph shows per cent inhibition of Ca2+ responses following treatment with selective blockers of glutamatergic and purinergic neurotransmitter receptors, including a combination of CNQX, DAPV, MCPG (GluR antagonists), suramin and MCPG. The results implicate both glutamate and ATP neurotransmitter signalling. P=0.3, n=6 cells from six dishes, *1P=0.03, n=4 cells from four dishes, **P=0.008, n=5 cells from five dishes, *2P=0.02, n=6 cells from six dishes, all paired t-test.