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Figure 5 | Molecular Pain

Figure 5

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 5

Pharmacological and biophysical dissection of TAT-CBD3A6K-mediated block of T-and R-type calcium currents in DRG neurons. (A) Representative T- (top) and R-type (bottom) current traces obtained from two separate DRG neurons evoked by 200 ms steps in 5 mV increments from −60 mV to +50 mV, from a holding potential of −90 mV. 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) Summary of the normalized conductance (G) versus voltage relations for DRG neurons with T- (filled squares) or R- (open squares) type calcium currents. The dotted line at −10 mV highlights the clear discrimination in conductances between T- and R-type currents. (C) Representative currents, evoked by a ramp depolarizations from −60 mV to +20 mV for 2 s, illustrating the presence of both T- and R-type currents in the same DRG neuron before (left trace) and 2 min after application 10 μM TAT-CBD3A6K (right trace)

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