The depolarization of skeletal muscle cells is caused by an elevation in extracellular potassium (K+). Initially, this depolarization brings the muscle cells closer to the threshold, making spontaneous action potentials and contractions more likely to occur. As the depolarization becomes more pronounced, the cells become refractory because more sodium (Na+) channels become inactivated. As a result, the cells are unable to generate action potentials and contract in response to action potentials in their motor axons.

During the latter part of the action potential and the afterhyperpolarization period, the cell can generate a second action potential, but a stronger stimulus is required. This period is known as the relative refractory period. In the early stages of the relative refractory period, some Na+ channels are still voltage inactivated, but enough channels in the closed state have the potential to open when the membrane is depolarized, allowing for the generation of an action potential if stimulated. However, a stronger stimulus than normal is needed to recruit the critical number of Na+ channels required to trigger an action potential. Throughout the relative refractory period, there is an increased conductance to potassium (K+), which counteracts membrane depolarization. This elevated K+ conductance persists during the afterhyperpolarization and contributes to the duration of the relative refractory period.

The transmission of information along neuronal pathways is fundamental to the functioning of the nervous system. Neurons generate action potentials to propagate down their axons without diminishing in size, ultimately triggering neurotransmitter release from presynaptic terminals. This section discusses how action potentials propagate along an axon and how the characteristics of the axon impact this propagation. The mechanism by which they trigger transmitter release is addressed separately.

Passive conduction alone cannot effectively transport a signal from one end of an axon to the other, unless the axon is very short in length. Neurons with short axons, such as those in the eye's retina, can rely on passive conduction due to the minimal distance between neurons. However, in most cases, axons are much longer than their length constant. Some axons can be over 1 meter long, such as those of motor neurons, making them hundreds of times their length constant. Nevertheless, when recording from different points along a typical axon, the shape and size of the action potential remain consistent as it travels along the fiber. This is because the action potential regenerates itself during active propagation along the axon.
Theelevationinextracellular[K+]causesdepolarizationofskeletalmusclecells.Initially,thedepolarizationbringsmusclecellsclosertothreshold,andsospontaneousactionpotentialsandcontractionsaremorelikelytooccur.Asdepolarizationofthecellsbecomesmoremarked,thecellsbecomerefractorybecauseincreasingnumbersofNa+ channelsbecomeinactivated.Consequently,thecellsbecomeunabletofireactionpotentialsandarenotabletocontractinresponsetoactionpotentialsintheirmotoraxons.
During the latter part of the action potential, and during the afterhyperpolarization period, the cell is able to fire a second action potential, but a stimulus stronger than normal is required. This period is called the relative refractory period. Early in the relative refractory period, before the
CHAPTER 5 Generation and Conduction of Action Potentials membrane potential has returned to the resting potential level, some Na+ channels are still voltage inactivated, but there are enough in the closed state (and therefore have the potential to open when the membrane is depolarized) to support the generation of an action potential if they are stimulated to open. However, a stimulus stronger than normal is necessary to recruit the critical number of Na+ channels needed to trigger an action potential (i.e., the reduction in the total number of available Na+ channels is countered by increasing the probability of opening). Throughout the relative refractory period, conductance to K+ is elevated, which opposes depolarization of the membrane. This increase in K+ conductance continues throughout the afterhyperpolarization and accounts for most of the duration of the relative refractory period.
Conduction of Action Potentials
Fundamental to nervous system function is the transmission of information along neuronal pathways. To accomplish this, neurons generate action potentials that propagate down the length of their axon without decrement in size in order to trigger neurotransmitter release from the presynaptic terminals. How action potentials propagate down an axon and how the characteristics of the axon affect this propagation are discussed in this section. How they trigger transmitter release is covered in
Action Potential as a Self-Reinforcing Signal
Passive conduction will not transport a signal from one end of an axon to the other unless the axon is very short (i.e., on the order of its length constant) because passively conducted signals decrease in size rapidly with distance from their origin. Neurons with such short axons exist; for example, in the retina of the eye, the distance from one neuron to the next is so small that electrotonic (passive) conduction is sufficient. However, in most cases, axons are many times longer than their length constant. In fact, they can be up to 1 m or more in length (e.g., those of motor neurons) and thus hundreds of times their length constant. Nonetheless, if researchers were to record from points along a typical axon, they would find that as the action potential arrives at successive points traveling along the axon, its shape and size remain constant. This is because the action potential regenerates itself as it is conducted along the fiber and thus is said to be actively propagated.