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Role of sodium channel Nav1.6 on high frequency firing C-tactile fibers
  CBN (Computational Biology and Neurocomputing) seminars

Thursday 05 September 2013
from 14:00 to 15:00
at RB35
Speaker : Michail Pantourakis (CB, KTH)
Abstract : 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.

Nordita  | Last modified 03 September 2013 14:15  |  HELP