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FIGURE 4–2. Opening of ion channels gives rise to the action potential.The upper traces show the two principal currents shaping the action potential, sodium (Na+) and potassium (K+) currents. Once a neuron reaches threshold for firing an action potential, voltage-activated Na+ channels open, giving rise to a rapid inward Na+ current and to the rapid rising phase of the action potential (green trace; membrane potential, EM). Once the membrane is depolarized, Na+ channels rapidly inactivate, reducing the Na+ current (purple trace) and thereby contributing to the falling phase of the action potential. Then, outward K+ current (yellow trace) activates, driving the falling phase of the action potential. K+ channels are slow to open but stay open for much longer than Na+ channels, pulling the EM back to the resting level. ENa and EK represent the reversal potentials for Na+ and K+, respectively, to which the opening of channels drives the membrane potential (EM). The lower schematic shows the local circuit currents that underlie the propagation of the action potential. The intense loop on the left spreads the depolarization to the right into unexcited membrane, which then renews the cycle, depolarizing the next segment and thereby propagating the action potential.Source. Reprinted from Hille B, Catterall WA: "Electrical Excitability and Ion Channels," in Basic Neurochemistry: Molecular, Cellular and Medical Aspects, 7th Edition. Edited by Siegel GJ, Albers RW, Brady S, Price DL. Burlington, MA, Elsevier Academic, 2006, pp. 95–109. Copyright 2006. Used with permission from Elsevier.

FIGURE 4–3. Action potential conduction in myelinated axon.Panel A. Schematic of a myelinated axon. Oligodendrocytes produce the insulating myelin sheath that surrounds the axon in segments. Myelination restricts current flow to the gaps between myelin segments, the nodes of Ranvier, where sodium (Na+) channels are concentrated. The result is a dramatic enhancement of the conduction velocity of the action potential. Panel B. Because Na+ channels are activated by membrane depolarization and also cause depolarization, they have regenerative properties. This underlies the "all-or-nothing" properties of the action potential and also explains its rapid spread down the axon. The action potential is an electrical wave; as each node of Ranvier is depolarized, it in turn depolarizes the subsequent node. Panel C. The Na+ current underlying the action potential is shown in three successive images at 0.5-millisecond intervals and corresponds to the current traces in Panel B. As the action potential (red shading) travels to the right, Na+ channels go from closed to open to inactivated to closed. In this way, an action potential initiated at the initial segment of the axon conducts reliably to the axon terminals. Because Na+ channels temporarily inactivate after depolarization, there is a brief refractory period following the action potential that blocks backward spread of the action potential and thus ensures reliable forward conduction.Source. Reprinted from Purves D, Augustine GJ, Fitzpatrick D, et al. (eds): Neuroscience, 3rd Edition. Sunderland, MA, Sinauer Associates, 2004, p. 64. Used with permission.

FIGURE 4–4. Intrinsic properties determine neuronal responses.Many CNS neurons respond differently to the same inputs, depending on their level of depolarization. Panel A. Thalamic neurons spontaneously generate bursts of action potentials, resulting from interactions between an inward pacemaker current and a calcium (Ca2+) current. Depolarization of these neurons changes their firing to a tonic mode. Panel B. Action potential bursts at higher time resolution from trace in Panel A. Panel C. Higher time resolution of currents in the tonic mode from Panel A. Ih and IT = the currents through a hyperpolarization-activated channel and a T-type calcium channel, respectively.Source. Reprinted from McCormick DA: "Membrane Potential and Action Potential," in Fundamental Neuroscience, 2nd Edition. Edited by Squire LR, Roberts JL, Spitzer NC, et al. San Diego, CA, Academic Press, 2003, pp. 139–161. Copyright Elsevier 2004. Used with permission.

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