Role of sodium channel Nav1.6 on high frequency firing C-tactile fibers

by Michail Pantourakis (CB, KTH)

Thursday 5 Sept 2013, 14:00 → 15:00 Europe/Stockholm

RB35

Whilst acute pain can be quite effectively treated by anesthetics and analgesics, complete relief from chronic pain has not been achieved in most cases. Since recent experimental findings have suggested a correlation between neuropathic pain cases, high frequency firing and sodium resurgent current, usually mediated by Na¬V1.6, we turn our attention on the C-tactile (CT) subgroup of nociceptors that naturally exhibit these features. Therefore, in the present work we build a spatial CT axon model and focus on the role of the Na¬V1.6 resurgent current, described by a multistate Markov model. Although high frequency spike trains (100-140 Hz) can be propagated by the axon, the main contributing sodium current is the rapidly activating and inactivating Na¬V1.7 and not Na¬V1.6. Surprisingly, the simulations show reduced firing frequencies in the presence of Na¬V1.6, and reduced conduction failure in its absence. Moreover, the seemingly opposing effects on the Na¬V1.6 dynamics of two potassium currents, K¬¬dr and KA, further illustrate the detrimental effect of the resurgent current on both the firing rate and the conduction of spike trains.