Chapter 7: Electrical Excitability and Action Potentials

The action potential is presented as a rapid, stereotyped change in membrane voltage that propagates along the axon, initiated when stimulation reaches threshold and depolarizes the membrane sufficiently to open voltage-gated sodium channels. The rising phase of the action potential reflects the inward sodium current that causes rapid depolarization, while the falling phase results from sodium channel inactivation and the opening of voltage-gated potassium channels that repolarize the membrane. The chapter explains the absolute and relative refractory periods, which determine the maximum firing frequency of neurons and the unidirectional propagation of action potentials. Particular attention is given to the role of myelin and Nodes of Ranvier in enabling saltatory conduction, which increases conduction velocity while conserving metabolic energy. The relationship between membrane capacitance and resistance is detailed to show how passive electrical properties affect voltage changes and signal propagation. The chapter connects these biophysical mechanisms to synaptic transmission, explaining how action potentials arriving at the presynaptic terminal trigger the opening of voltage-gated calcium channels, leading to neurotransmitter release and postsynaptic signaling. Clinical and pharmacological examples, including local anesthetics that block voltage-gated sodium channels and toxins affecting potassium channels, illustrate how disruption of normal electrical excitability underlies neurological dysfunction. By integrating molecular mechanisms with systems-level function, this chapter demonstrates how action potentials enable neurons to generate, conduct, and transmit signals rapidly across distances.