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Figure 2 | Molecular Pain

Figure 2

From: Spinal morphine but not ziconotide or gabapentin analgesia is affected by alternative splicing of voltage-gated calcium channel CaV2.2 pre-mRNA

Figure 2

Development of thermal and mechanical hypersensitivity after peripheral nerve injury in wild-type and e37b-only mice. A, Paw withdrawal latency to noxious thermal stimuli applied to hindpaws ipsilateral (I) and contralateral (C) to the injury in wild-type (WT) and e37b-only (e37b) mice (Hargreaves method). Latencies were measured at the time points indicated before and after injury (at time 0). P values comparing latencies in WT and e37b-only mice were > 0.05 at all time points except at day 21 (P = 0.015). At days -8, -7, -1, 0, 3, 5, 7, 14, 21 and 28, P values were 0.37, 0.81, 0.07, 0.52, 0.85, 0.74, 0.90, 0.30, 0.71, and 0.87 contralateral; P values were 0.72, 0.81, 0.10, 0.87, 0.72, 0.28, 0.29, 0.83, 0.015 and 0.16 for ipsilateral. B, Paw withdrawal thresholds to mechanical stimuli applied to hindpaws in WT and e37b-only mice (von Frey filaments). The 50% paw withdrawal threshold from the same side paw compared between WT and e37b-only mice: At days -8, -7, -1, 0, 3, 5, 7, 14, 21 and 28, P values were: 0.26, 0.44, 0.29, 0.63, 0.35, 0.28, 0.60, 0.21, 0.05 and 0.18 for contralateral; P values were 0.37, 0.72, 0.74, 0.65, 0.47, 0.24, 0.89, 0.67, 0.36 and 0.57 for ipsilateral. CaV2.2 currents measured from capsaicin-responsive neurons of dorsal root ganglia L4, L5 and L6. Total calcium channel currents were recorded and current voltage-relationships generated in the absence and in the presence of ω-conotoxin GVIA (D). CaV2.2 current was generated by toxin-subtraction (C). There is no consistent difference between CaV2.2 current and non-CaV2.2 currents (CgTx-resistant) measured under the different conditions. Only cells responding to 1 μM capsaicin were analyzed. Values are average ± SE. Student’s two-tailed t-test.

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