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Figure 6 | Molecular Pain

Figure 6

From: CRMP-2 peptide mediated decrease of high and low voltage-activated calcium channels, attenuation of nociceptor excitability, and anti-nociception in a model of AIDS therapy-induced painful peripheral neuropathy

Figure 6

Characterization of TAT-CBD3A6K-mediated inhibition of T- and R-type calcium currents. (A) Representative family of traces from a DRG neuron with both T- and R-type calcium currents before (left), 2 min (middle) and 5 min (right) after addition of 10 μM TAT-CBD3A6K. Currents were elicited in response to the voltage protocol described in the legend to Figure 5A. To isolate T- and R-type calcium currents, the extracellular bath solution contained 5 mM Nifedipine (Nif), 200 nM ω-Agatoxin IVA (Aga) and 500 nM ω-Conotoxin GVIA (CTX) to block L-, P/Q-, and N-type calcium currents, respectively. (B, C) Time course of TAT-CBD3A6K mediated inhibition (“run-down”) of T-type (B) and R-type (C) calcium currents. Time course of inhibition is shown as averaged normalized current density (pA pF-1) before peptide addition and at intervals of 30 s for 5 min. Averaged values are shown with standard error for 4–6 control cells and 4 cells following addition of 10 μM TAT-CBD3A6K. The asterisk denotes statistical significance (p < 0.05; Student’s t-test) compared to the corresponding control time point. Some error bars are smaller than the symbols. Data represent mean ± SEM from n = 3–6 cells at each time point except for n = 2 the 4 min time point for T-type currents in the presence of peptide

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