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Figure 4 | Molecular Pain

Figure 4

From: Contribution of TRPC3 to store-operated calcium entry and inflammatory transductions in primary nociceptors

Figure 4

Functional coupling between TRPC3 and UTP/P2Y2 signaling in DRG neurons. (A) The addition of 100 μM UTP for 7 minutes to the calcium-free perfusion solution activates P2Y2 receptors, which initiate both SOCE and ROCE responses. The addition of Gd3+ removes the Orai component of the UTP-evoked response, which accounts for approximately 35% of the overall calcium influx (n = 17-19, P < 0.05). (B) The blockade of TRPC3 specifically with Pyr10 (10 μM, 15 min) resulted in a drastic decrease of UTP-evoked calcium entry, resulting in 60% inhibition (n = 25-28, P < 0.001). (C) shRNA-mediated knockdown of TRPC3 induced in similar decrease of P2Y2-mediated calcium entry (n = 34-46, P < 0.0001). (D) Heterologous overexpression of TRPC3 (OE) resulted in 90% increase of calcium influx in the UTP response, indicating a strong link between TRPC3 activity and P2Y2 transduction (n = 24-45, P < 0.001).

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