The action potential is a self-propagating change in membrane voltage conducted sequentially along the axon of a neuron that transmits information from the neuron cell body or sensory ending to the axon terminal. The action potential is initiated either as the consequence of summation of local electronic potentials in the region where the axon arises from the neuron cell body (axon hillock), or as a result of a sufficiently large generator potential in the sensory ending. Once initiated, the action potential is conducted without change in magnitude along the axon until it invades the axon terminal and causes release of quanta of neurotransmitter molecules.
To understand the action potential it is necessary to understand the resting membrane potential. To record the resting membrane potential and the action potential one electrode is inserted into the cell while a second electrode remains outside the cell. The voltage potential between the two electrodes is amplified and measured. For most neurons the measured resting membrane potential is from -60 to -70 millivolts (mV); the inside of the cell is negative relative to the outside of the cell.
The resting membrane potential is determined by the relative distribution of positively or negatively charged ions near the extracellular and intracellular surfaces of the cell membrane. Positive sodium (Na+) and potassium (K+) ions and negative chloride (Cl-) and organic (A-) ions are important for both the resting membrane potential and the action potential. The positively charged ions are called cations, and the negatively charged ions are called anions. The organic anions are mostly proteins and organic acids.
During the resting state Na+ and Cl- have higher extracellular than intracellular concentrations, and K+ and A- are more highly concentrated within the cell. The organic ions never leave the intracellular compartment, and in most neurons Cl- is relatively free to pass through the membrane. Three factors contribute to determining the ionic distribution across the membrane. The first factor is the relative permeability of the membrane to each ion species. The second factor is the concentration gradient of each ion species. The third factor is the electromotive force created by the separation of charges across the semipermeable membrane.
Because the inside of the cell is negative relative to the outside, and there is a lower intracellular concentration of Na+, the sodium cations would flood into the cell if the membrane were freely permeable to Na+. At rest, however, the cell membrane is not freely permeable to Na+. Permeability of a membrane to any given ion species is controlled by the number of membrane channels available for that particular species. Membrane channels are made of proteins that extend from the extracellular to the intracellular surface of the membrane (i.e., they are membrane-spanning). The membrane channels may be always open, or nongated, or open only under certain conditions. Channels that open or close depending on conditions are called gated channels. Whether gated channels are open or closed depends on the conformation of the proteins that form the walls of the channel. When the neuron membrane is at rest the gated channels for Na+ are closed. The Na+ that does enter flows through the nongated, nonspecific channels in the membrane, but it is actively extruded from the cell by the sodium-potassium pump. This pump is made of carrier proteins and uses metabolic energy supplied by adenosine triphosphate (ATP). Na+ and K+ are linked in transmembrane transportation such that three Na+ ions are transported out of the cell for every two K+ ions that are transported into the cell. The Na+-K+ pump maintains the in-tracellular and extracellular concentrations of these ions, which is necessary for homeostatic osmotic equilibrium across the cell membrane as well as creation of the resting membrane potential.
During the resting state the membrane channels do not allow movement of Na+ into the cell. However, some Na+ does enter the cell through nonspecific membrane channels. Na+ does this because it has a higher concentration outside than inside and, therefore, flows down its concentration gradient. Additionally, the electromotive force created by the relative intracellular negativity propels Na+ inward. The sodium-potassium ATP-coupled pump counteracts the influx of Na+ ions in the resting state.
The membrane is also not fully permeable to K+ in the resting state, but K+ ions are, compared to Na+ ions, freer to move through the cell membrane. That is, the neuron membrane is more permeable to K+ than to Na+. For this reason K+ moves more readily down its concentration gradient than Na+, and the resting membrane potential is, therefore, closer to the K+ equilibrium potential than the Na+ equilibrium potential.
To summarize, in the resting state the paucity of open membrane channels for Na+ and K+ and the Na+-K+ pump serve to maintain an excess of extracellular Na+ and intracellular K+. The magnitude of the resting membrane potential is the result of the degree of separation of these cations and the presence of the organic anions within the cell. Because the membrane is more permeable to K+ than Na+, the resting membrane potential more closely approximates the equilibrium potential for K+ than for Na+.
The Na+ and K+ channels are voltage-gated. This means that a change in voltage across the membrane changes the conformation of the channel protein to either open or close the channel. If the membrane depolarizes and the membrane potential becomes more positive, the Na+ channels begin to open. On dendrites and cell bodies, channels are opened by neurotransmitters released at the synapse from other cells. The neurotransmitters bind to receptors on the target neuron and open chemically gated ion channels. If the neurotransmitter is excitatory, the postsynaptic membrane is slightly depolarized in the area of the synapse. This depolarization is less than required for generation of an ac tion potential. However, depolarizing excitatory postsynaptic potentials (EPSPs) sum at the axon hillock with hy-perpolarizing inhibitory postsynaptic potentials (IPSPs). If the resulting change in membrane polarity at the hillock is a depolarization that exceeds about 10 mV an action potential is initiated.
Depolarization at the axon hillock causes voltage-gated Na+ channels to open. The number of Na+ channels opened by the depolarization is proportional to the amount of positive change in membrane potential until threshold for action potential initiation is exceeded, at which time essentially all of the Na+ channels in the area of threshold depolarization open and Na+ rushes into the axon. The membrane potential then moves rapidly (about 0.5 ms) toward Na+ equilibrium potential until it becomes about +55 mV. This is the rising phase of the action potential; when it reaches its peak, Na+ channels close and voltage-gated K+ channels open. K+ leaves the cell and, in combination with decreased Na+ conductance, reverses the depolarization. The K+ channels stay open long enough not only to return the membrane potential to its resting level, but to cause a brief (about 2 ms) overshoot hyperpolarization. During the early part of the hyperpolarizing phase of the action potential, Na+ channels can not reopen and another action potential can not be generated. This is known as the absolute refractoryperiod. This prevents action potentials from sum-mating. As the membrane continues to repolarize, an action potential can be generated if a stronger than normal stimulus is applied to the axon. This is known as the relative refractory period. Within 2.5 ms after peak depolarization of the action potential, the resting Na+-K+ concentrations are restored and the system is ready for reactivation.
The action potential propagates because the ionic current flow at one point of the membrane causes changes in current flow in the adjacent membrane toward the axon terminal. The current flow changes the transmembrane voltage potential and opens Na+ channels. The entire sequence just described is then repeated. In myelinated axons, the current flow occurs only at the nodes of Ranvier. In addition to lacking the electrical insulation provided by myelin, the nodes of Ranvier also have a far greater concentration of Na+ channels than do the parts of the axon covered by myelin. The result of the presence of myelin is that the action potential jumps from one node to the next (saltatory conduction). This produces more rapid conduction of the action potential than is possible in nonmyelinated axons.
Koester, J. (1991a). Membrane potential. In E. R. Kandel, J. H.
Schwartz, & T. M. Jessell (Eds.), Principles of neural science
(3rd ed., pp. 81-94). New York: Elsevier. Koester, J. (1991b). Voltage-gated ion channels and the generation of the action potential. In E. R. Kandel, J. H. Schwartz, & T. M.
Jessell (Eds.), Principles of neural science (3rd ed., pp. 104118). New York: Elsevier.
Siegelbaum, S. S., & Koester, J. (1991). Ion channels. In E. R. Kandel, J. H. Schwartz, & T. M. Jessell (Eds.), Principles of neural science (3rd ed., pp. 66-79). New York: Elsevier.
Shepherd, G. M. (1994). The membrane potential: The action potential. In Neurobiology (3rd ed., pp. 87-121). New York: Oxford University Press.
Smock, T. K. (1999). Communication among neurons: The membrane potential. In Physiological psychology: Aneuroscience approach (pp. 47-87). Upper Saddle River, NJ: Prentice Hall.
Michael L. Woodruff
East Tennessee State University
Was this article helpful?
Here's How You Could End Anxiety and Panic Attacks For Good Prevent Anxiety in Your Golden Years Without Harmful Prescription Drugs. If You Give Me 15 minutes, I Will Show You a Breakthrough That Will Change The Way You Think About Anxiety and Panic Attacks Forever! If you are still suffering because your doctor can't help you, here's some great news...!