Key Concepts of Section 22.2

Key Concepts of Section 22.2

Voltage-Gated Ion Channels and the Propagation of Action Potentials

  • Action potentials are sudden membrane depolarizations followed by rapid repolarization.

  • An action potential results from the sequential opening and closing of voltage-gated Na+ and K+ channels in the plasma membrane of neurons and muscle cells (excitable cells; see Figure 22-10).

  • Opening of voltage-gated Na+ channels permits influx of Na+ ions for about 1 ms, causing a sudden large depolarization of a segment of the membrane. The channels then close and become unable to open (refractory period) for several milliseconds, preventing further Na+ flow (see Figure 22-10).

  • As the action potential reaches its peak, opening of voltage-gated K+ channels permits efflux of K+ ions, which repolarizes and then hyperpolarizes the membrane. As these channels close, the membrane returns to its resting potential (see Figures 22-2 and 22-9).

  • The excess cytosolic cations associated with an action potential generated at one point on an axon spread passively to the adjacent segment, triggering opening of voltage-gated Na+ channels in the vicinity and thus propagation of the action potential along the axon.

  • Because of the absolute refractory period of the voltage-gated Na+ channels and the brief hyperpolarization resulting from K+ efflux, the action potential is propagated in one direction only, toward the axon termini (see Figure 22-12).

  • Voltage-gated Na+ channels are monomeric proteins containing four domains that are structurally and functionally similar to each of the subunits in the tetrameric voltage-gated K+ channels. Each domain or subunit in voltage-gated cation channels contains six transmembrane α helices and a nonhelical P segment that forms the ion-selectivity pore (see Figure 22-13).

  • Opening of voltage-gated channels results from movement of the positively charged S1–S4 paddles toward the extracellular side of the membrane in response to a depolarization of sufficient magnitude (see Figure 22-14).

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  • Closing and inactivation of voltage-gated cation channels result from movement of a cytosolic “ball” segment into the open pore (see Figure 22-10).

  • While the voltage sensor and inactivation gate of voltage-gated K+ channels and voltage-gated Na+ channels are similar, the structure of the selectivity filter is different, and provides specificity for the type of ion that is conducted through the channel.

  • Myelination, which increases the rate of impulse conduction up to a hundredfold, permits the close packing of neurons characteristic of vertebrate brains.

  • In myelinated neurons, voltage-gated Na+ channels are concentrated at the nodes of Ranvier. Depolarization at one node spreads rapidly with little attenuation to the next node, so that the action potential jumps from node to node (see Figure 22-16).

  • Myelin sheaths are produced by glial cells that wrap themselves in spirals around neurons. Oligodendrocytes produce myelin for the CNS; Schwann cells, for the PNS (see Figure 22-17).

  • The field of optogenetics is revolutionizing the study of neural circuits. It involves the genetic expression of light-activated cation channels, called channelrhodopsins, in neurons, and the use of light to specifically activate or inhibit that population of neurons. In this way, neuroscientists can directly link specific neural circuits with specific behaviors.