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Figure 1 | Molecular Pain

Figure 1

From: Familial hemiplegic migraine CaV2.1 channel mutation R192Q enhances ATP-gated P2X3 receptor activity of mouse sensory ganglion neurons mediating trigeminal pain

Figure 1

Functional characterization and expression of P2X 3 receptors in WT and R192Q KI trigeminal ganglion neurons. A, Representative current traces induced by α,β-meATP (10 μ M, 2-s application) on WT and KI neurons. B, Dose-response curves for WT (n = 18, filled circles) and KI (n = 17, open circles) cells. * p = 0.04, ** p = 0.035, ***p = 0.03. Note larger responses of α,β-meATP-mediated currents on KI neurons with respect to WT, as the dose-effect plot is shifted upwards for KI neurons. C, Rise time (left; expressed as τon calculated on the 10-90% response rise), desensitization onset (middle; expressed as the first time constant, τfast, of current decay) and recovery from desensitization (right; expressed as% of control amplitude in a paired pulse agonist application) of P2X3 receptor currents are similar for WT and KI neurons. All responses were evoked by α,β-meATP (10 μM, 2 s). n = 154 for WT and n = 183 for KI. D, Histograms show peak amplitude distribution of α,β-meATP (10 μ M)-induced P2X3 currents for WT (n = 414, open bars) and KI (n = 454, filled bars). E, Histograms show the distribution of current density (i.e., current amplitude normalized with respect to the neuronal capacitance, pA/pF) for WT (n = 414, open bars) and KI (n = 454, filled bars) neurons, indicating significantly higher α,β-meATP-evoked KI responses over a span of 15-35 pA/pF values compared to WT.

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