The Action Potential
(Nerve Impulse and Saltatory Conduction)
Action potentials are the electrical signals, or nerve impulses, by which information is conducted from one area to another within a single cell. The action potential is an all or none change in membrane potential in the body or axon of a neuron or within a muscle fiber. It either occurs fully or not at all and depends on the sodium channel. The function of action potentials is to conduct bits of information from one place to another. The action potential is initiated by one form of local potential, the electrotonic potential.
Conduction of the nerve impulse along the cell membrane depends on a series of local electrical events, each of which is triggered by the one immediately preceding it.
Depolarization of a patch of membrane causes a local interchange of ions with an adjacent patch, which, if sufficient to depolarize that patch to a threshold level, results in a full-fledged action potential there. This transfer of depolarization is generated by a current flow (C) created by the movement of positive charge (+)(ions) into an area of negative charge (-) and the extracellular surge of positive ions into the region of depolarization. The current spreads along the axon, seeking a pathway of least resistance; the higher the membrane resistance, the farther the current flows along the axon. The result is a self-propagating nerve impulse moving along the membrane without loss of speed or energy.
It is not sufficient that a nerve cell membrane be capable of simply firing an action potential; that potential must be conducted along the length of the membrane as well. In many cases that membrane is part of an axon, and that axon may be as long as 1 meter. Further, the conduction of the action potential must take place quite rapidly. How long does it take you to be aware of pain after you have stepped on a sharp object? Consideration of the mechanism for conduction of the action potential (nerve impulse) and structural factors that enhance the velocity of impulse conduction are considered.
In theory, the nerve impulse moves in both directions; in practice, it probably does not, as the patch behind the most recently depolarized area is recovering from the depolarized state and therefore still likely to be in a non-responsive or refractory state. The existence of such refractory periods immediately following the passage of impulses also explains why every axon has a maximum rate of impulse conduction beyond which it cannot conduct. Following the refractory state, the membrane returns to a resting potential.
Axons of the PNS greater than 1 micrometer in diameter have a lipoprotein-rich membrane coat called the myelin sheath. Produced and maintained by Schwann cells, myelin sheathes are interrupted at the interface between these cells. Such interruptions are called nodes of Ranvier, and here the axon is naked, making the nodes preferential sites for impulse generation and propagation. Myelin, being a fatty substance, resists the flow of current through it, and the number of Na+ channels in the underlying axonal cell membrane is limited. Where the myelin sheath is absent, at the node of Ranvier, the Na+ channels are packed into the membrane more densely than in any other region of the neuronal membrane. Nodes of Ranvier are also found in the CNS.
When excitation of a myelinated axon occurs, the action potential literally jumps from node to node (saltatory conduction; saltare, "to jump"). The intracellular current flow moves from one node to the next. The myelin sheath prevents the current from leaking back across the membrane as it is "booted" to the next node. The greater the distance between nodes, the faster the speed of conduction. In general, the larger the axon, the greater the impulse velocity.
Impulses in certain large, myelinated sensory and motor fibers may travel as fast as 100 meters per second (m/s); the smallest myelinated axons conduct impulses at 3 m/s or more. The more numerous non-myelinated axons -without nodes and therefore without saltatory conduction - conduct impulses more slowly.
The transmission of information in the nervous system depends on the generation of a resting potential that acts as a reserve of energy poised for release when the valve is turned on. Ionic channels act as the valve, controlling the energy in the ionic concentration gradient. The release of energy is seen either as local graded potentials or as propagated action potential that arise when local potentials reach threshold. Information is moved from one area to another as action potentials conducted by single cells. The information is integrated in neurons by the interaction of local potentials generated in response to the neurotransmitters released from depolarized nerve terminals.
In this system, information can be coded either as the rate of discharge in individual cells or axons or as the number and combination of active cells. Both of these are important mechanisms, for although the activity of the nervous system can be conveniently described in terms of the electrical activity of single cells, the combined activity of large numbers of cells and axons determines the behavior of the organism. Each type of alteration in neuronal or muscle cell physiology can produce symptoms or signs of short duration, transient disorders. The particular findings in a patient depend on which cells are altered. if the changes are in neurons that subserve sensation, there may be a loss of sensation or an abnormal sensation such as tingling, loss of vision, or "seeing stars." In other systems, there may be a loss of strength, twitching in muscles, loss of intellect, or abnormal behavior.
In all these cases, the physiologic alterations are not specific and may be the result of any one of a number of diseases. Transient disorders do not permit a pathologic or etiologic diagnosis. Any type of disease (vascular, neoplastic, inflammatory) may be associated with transient changes. Therefore, the pathology of a disorder cannot be deduced when its temporal profile is solely that of transient episodes.
Conduction of the nerve impulse along the cell membrane depends on a series of local electrical events, each of which is triggered by the one immediately preceding it.
Depolarization of a patch of membrane causes a local interchange of ions with an adjacent patch, which, if sufficient to depolarize that patch to a threshold level, results in a full-fledged action potential there. This transfer of depolarization is generated by a current flow (C) created by the movement of positive charge (+)(ions) into an area of negative charge (-) and the extracellular surge of positive ions into the region of depolarization. The current spreads along the axon, seeking a pathway of least resistance; the higher the membrane resistance, the farther the current flows along the axon. The result is a self-propagating nerve impulse moving along the membrane without loss of speed or energy.
It is not sufficient that a nerve cell membrane be capable of simply firing an action potential; that potential must be conducted along the length of the membrane as well. In many cases that membrane is part of an axon, and that axon may be as long as 1 meter. Further, the conduction of the action potential must take place quite rapidly. How long does it take you to be aware of pain after you have stepped on a sharp object? Consideration of the mechanism for conduction of the action potential (nerve impulse) and structural factors that enhance the velocity of impulse conduction are considered.
In theory, the nerve impulse moves in both directions; in practice, it probably does not, as the patch behind the most recently depolarized area is recovering from the depolarized state and therefore still likely to be in a non-responsive or refractory state. The existence of such refractory periods immediately following the passage of impulses also explains why every axon has a maximum rate of impulse conduction beyond which it cannot conduct. Following the refractory state, the membrane returns to a resting potential.
Axons of the PNS greater than 1 micrometer in diameter have a lipoprotein-rich membrane coat called the myelin sheath. Produced and maintained by Schwann cells, myelin sheathes are interrupted at the interface between these cells. Such interruptions are called nodes of Ranvier, and here the axon is naked, making the nodes preferential sites for impulse generation and propagation. Myelin, being a fatty substance, resists the flow of current through it, and the number of Na+ channels in the underlying axonal cell membrane is limited. Where the myelin sheath is absent, at the node of Ranvier, the Na+ channels are packed into the membrane more densely than in any other region of the neuronal membrane. Nodes of Ranvier are also found in the CNS.
When excitation of a myelinated axon occurs, the action potential literally jumps from node to node (saltatory conduction; saltare, "to jump"). The intracellular current flow moves from one node to the next. The myelin sheath prevents the current from leaking back across the membrane as it is "booted" to the next node. The greater the distance between nodes, the faster the speed of conduction. In general, the larger the axon, the greater the impulse velocity.
Impulses in certain large, myelinated sensory and motor fibers may travel as fast as 100 meters per second (m/s); the smallest myelinated axons conduct impulses at 3 m/s or more. The more numerous non-myelinated axons -without nodes and therefore without saltatory conduction - conduct impulses more slowly.
The transmission of information in the nervous system depends on the generation of a resting potential that acts as a reserve of energy poised for release when the valve is turned on. Ionic channels act as the valve, controlling the energy in the ionic concentration gradient. The release of energy is seen either as local graded potentials or as propagated action potential that arise when local potentials reach threshold. Information is moved from one area to another as action potentials conducted by single cells. The information is integrated in neurons by the interaction of local potentials generated in response to the neurotransmitters released from depolarized nerve terminals.
In this system, information can be coded either as the rate of discharge in individual cells or axons or as the number and combination of active cells. Both of these are important mechanisms, for although the activity of the nervous system can be conveniently described in terms of the electrical activity of single cells, the combined activity of large numbers of cells and axons determines the behavior of the organism. Each type of alteration in neuronal or muscle cell physiology can produce symptoms or signs of short duration, transient disorders. The particular findings in a patient depend on which cells are altered. if the changes are in neurons that subserve sensation, there may be a loss of sensation or an abnormal sensation such as tingling, loss of vision, or "seeing stars." In other systems, there may be a loss of strength, twitching in muscles, loss of intellect, or abnormal behavior.
In all these cases, the physiologic alterations are not specific and may be the result of any one of a number of diseases. Transient disorders do not permit a pathologic or etiologic diagnosis. Any type of disease (vascular, neoplastic, inflammatory) may be associated with transient changes. Therefore, the pathology of a disorder cannot be deduced when its temporal profile is solely that of transient episodes.