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Figure 8 | Molecular Pain

Figure 8

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 8

Schematic summarizing effects of CBD3A6K peptide on excitability and T- and R-type calcium channels. The figure shows a tentative model of the effects of CBD3A6K on an action potential recorded from a primary afferent neuron exhibiting T-type LVACC (arrowheads) and R-type (CaV2.3) HVACC (arrows). (A) The action potential was elicited by the injection of a depolarizing current. CBD3 blocks the T- but not R-type currents (B) while CBD3A6K has defined blocking effects on both the T- and the R-type currents (C). T-type calcium currents generally make little contribution to the rising phase of action potentials because their activation kinetics are slower than sodium channels. However, R-type calcium channels typically begin to be activated near the peak of the action potential and this calcium current is largest during the falling phase, when channels have been opened and the driving force on calcium increases. Whether the rapid calcium entry via R-type channels contributes to the activation of large conductance calcium-activated potassium channels is unknown

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