Upsetting the balance among membrane channels can produce hyperexcitability or inexcitability

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Disorders of excitable membranes provide a fascinating opportunity to link basic physiology with clinical neurology. Understanding disorders of membrane excitability enhances knowledge of the complex interactions among ion channels that control membrane polarization. In skeletal muscle the important channels are chloride, sodium, and potassium.1–3 For axons, the key players are voltage gated sodium and potassium channels. Sodium channels carry the inward current that triggers and forms the rapid depolarizing phase of an action potential. Potassium current opposes membrane depolarization to impair action potential genesis and hasten repolarization that terminates the action potential. The diversity of neuronal voltage-gated channels enables cells to have unique electrical properties.4 For both potassium and sodium channels, many genes encode different versions (isoforms) of the channel proteins. A single gene encodes for the entire sodium channel protein, whereas potassium channels are formed by four subunits. A potassium channel can be formed by four copies of the same subunit or by a mix of several subunits. Hence, an enormous number of structurally distinct potassium channels can be formed through combinations of available subunits. The peripheral nociception system shows that selection of specific ion channels molds how classes of neurons work. The SCN9A gene …