Voltage-gated sodium, potassium, and calcium channels are crucial for generating electrical signals in excitable cells. Key Points: Voltage-gated Na channels: Opening leads to a rapid influx of Na?, causing depolarization.Inactivation and refractory period: Voltage-gated Na channels close in a two-step process: An inactivating gate blocks the channel pore but doesn’t close the channel. This typically occurs even before the membrane voltage repolarizes, and it can produce a refractory period.After the membrane voltage repolarizes, the activation gate closes, resetting the channel. Voltage-gated K channels: Opening allows K? to leave the cell, leading to repolarization and hyperpolarization. Also called delayed rectifier channels.Voltage-gated Ca channels: Contribute to action potentials in cardiac muscle cells but have other essential roles in neurons and skeletal muscle cells that we will discuss later.There are many subtypes of the voltage-gated Na, K, and Ca channels that differ in properties such as threshold voltage, gating duration, and conductivity. Question The drug lidocaine binds to a site in the inner pore of voltage-gated sodium channel. The drug accesses the site when the channel is open. Once bound, lidocaine physically blocks ion flow and stabilizes the channel in an inactivated state. Based on this, which of the following best describes the expected effect of lidocaine on neuronal action potentials? Action potentials will have a faster falling phase, since sodium channels enter inactivation more quickly. Action potentials will have a slower rising phase but normal amplitude, since sodium influx is partially reduced. Action potentials will have normal timing but reduced amplitude, since fewer sodium channels are available. During action potential generation, the membrane will begin to depolarize but fail to fully generate.