Rrp

Figures The Hodgkin-Huxley model accounts for axonal excitability. (a) From top to bottom, applied current Iapp, membrane potential Vm, and each of the gating variables are plotted vs time. Curves were derived from the Hodgkin-Huxley model at 6°C. The rapid activation of the m gate underlies the action potential in response to this brief current pulse. The slower inactivation of the h gate and activation of the n gate repolarize the membrane a few milliseconds later. The duration of the absolute and relative refractory periods (ARP and RRP, respectively) is controlled by the duration of h gate inactivation and n gate activation. (b) After a hyperpolarizing input, the Hodgkin-Huxley model (6°C, with enhanced density of the Na+ conductance) can produce a rebound spike (also known as anode break excitation). Data are plotted in the same order as in (a). Deactivation of the n gate and deinactivation of the h gate underlie this phenomenon.

Direction of Propagation

Spiking

Refractory Membrane Membrane

Charging Membrane

Charging Membrane

Figure 6 Propagation of the action potential in an unmyelinated axon. (Top) Schematic of the unmyelinated axon showing the sequence of events as an action potential propagates from left to right. The point of maximal Na+ flux characterizes the locus where Vm is greatest. Positive charge from this point spreads to the right, gradually depolarizing the membrane on the leading edge of the action potential until threshold is reached. At the trailing edge of the action potential, to the left, the membrane is refractory. (Bottom) "Snapshot" of Vm plotted vs axial distance for the propagating action potential, with an assumed conduction velocity of 20 m/sec. Note that the form of the action potential is reversed when plotted vs distance rather than time.

Figure 6 Propagation of the action potential in an unmyelinated axon. (Top) Schematic of the unmyelinated axon showing the sequence of events as an action potential propagates from left to right. The point of maximal Na+ flux characterizes the locus where Vm is greatest. Positive charge from this point spreads to the right, gradually depolarizing the membrane on the leading edge of the action potential until threshold is reached. At the trailing edge of the action potential, to the left, the membrane is refractory. (Bottom) "Snapshot" of Vm plotted vs axial distance for the propagating action potential, with an assumed conduction velocity of 20 m/sec. Note that the form of the action potential is reversed when plotted vs distance rather than time.

Membrane potential reaches its peak value near the position of maximal Na+ flux. Adjacent, unexcited membrane (Fig. 6, right) is depolarized by positive current from the site of Na+ flux. Eventually, this depolarization is large enough that the membrane at the leading edge is excited as well. The membrane in the wake of the action potential is refractory (i.e., dominated by small GNa and large GK, and thus unable to spike) and thus unlikely to be reexcited. Elaborations of this model can account for saltatory conduction in myelinated axons.

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