This thesis determines how the recovery from inactivation is regulated by the molecular mechanism attributed to the various functional entities of the channels and what the role of individual subunits in this process. To answer this question, we determined the membrane potential dependence of recovery parameters in wide-type and mutant homotetrameric channels, and evaluated the recovery of heteromeric channels (containing mutant and wild-type subunits). The results showed that during the recovery from inactivation cooperativity exists between the subunits. Therefore, the result predicts the dominating role of mutant subunits in the time-course of transition from inactivated to closed/recovered state.