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In this work we have theoretically investigated how the action potentialgeneration and its associated intrinsic properties are affected in presence ofion channel blockers by adapting Gillepie's stochastic simulation technique ona very basic neuron of Hodgkin-Huxley type. With a simple extension of theHodgkin-Huxley Markov model we have mainly investigated three types of drugblocking mechanisms and showed that the major experimental and physiologicalobservations such as ionic currents, spiking frequency trends, change in actionpotential shape and duration, altered gating dynamics etc due to the presenceof ion channel blockers can be well reproduced. The nature of action potentialtermination process in presence of sodium and potassium channel blockers aredistinct and physiologically very different from each other. Channel blockershave distinct signatures on ionic currents. In presence of only sodium channelblockers the frequency of action potential generation falls off exponentiallywith increasing drug affinity, whereas in contrast, for only potassium channelblockers initially an enhanced spiking activity of action potential is foundfollowed by a gradual decrease of the spiking frequency as the drug affinityincreases. In case of dual type blockers with equal sodium and potassiumchannel binding affinity, the spiking frequency passes through maxima andminima due to the competition between channel number fluctuation and overallsodium and potassium conductances. We have found that sodium channel blockersshorten the duration of action potential while the potassium channel blockersdelay it. We have also shown how the ion channel blockers alter the gatingdynamics. Some experimental results of ion channel blocking in diverse systemshave been validated through our site selected binding scheme.

Effect Of Site Selective Ion Channel Blocking on Action Potential