This is known as depolarization , meaning the membrane potential moves toward zero. The electrical gradient also plays a role, as negative proteins below the membrane attract the sodium ion.
These channels are specific for the potassium ion. This is called repolarization , meaning that the membrane voltage moves back toward the mV value of the resting membrane potential. Repolarization returns the membrane potential to the mV value that indicates the resting potential, but it actually overshoots that value.
What has been described here is the action potential, which is presented as a graph of voltage over time in Figure 8. It is the electrical signal that nervous tissue generates for communication. That can also be written as a 0. To put that value in perspective, think about a battery. An AA battery that you might find in a television remote has a voltage of 1. The change seen in the action potential is one or two orders of magnitude less than the charge in these batteries.
In fact, the membrane potential can be described as a battery. A charge is stored across the membrane that can be released under the correct conditions. What happens across the membrane of an electrically active cell is a dynamic process that is hard to visualize with static images or through text descriptions.
View this animation to learn more about this process. And what is similar about the movement of these two ions? The question is, now, what initiates the action potential? The description above conveniently glosses over that point. But it is vital to understanding what is happening. The membrane potential will stay at the resting voltage until something changes. Instead, it means that one kind of channel opens. Whether it is a neurotransmitter binding to its receptor protein or a sensory stimulus activating a sensory receptor cell, some stimulus gets the process started.
Sodium starts to enter the cell and the membrane becomes less negative. The channels that start depolarizing the membrane because of a stimulus help the cell to depolarize from mV to mV.
This is what is known as the threshold. Any depolarization that does not change the membrane potential to mV or higher will not reach threshold and thus will not result in an action potential. Also, any stimulus that depolarizes the membrane to mV or beyond will cause a large number of channels to open and an action potential will be initiated. Because of the threshold, the action potential can be likened to a digital event—it either happens or it does not.
If the threshold is not reached, then no action potential occurs. Also, those changes are the same for every action potential, which means that once the threshold is reached, the exact same thing happens. Stronger stimuli will initiate multiple action potentials more quickly, but the individual signals are not bigger.
Thus, for example, you will not feel a greater sensation of pain, or have a stronger muscle contraction, because of the size of the action potential because they are not different sizes. The action potential is initiated at the beginning of the axon, at what is called the initial segment. Because of this, depolarization spreading back toward previously opened channels has no effect.
The action potential must propagate toward the axon terminals; as a result, the polarity of the neuron is maintained, as mentioned above. Propagation, as described above, applies to unmyelinated axons. When myelination is present, the action potential propagates differently. Because there is not constant opening of these channels along the axon segment, the depolarization spreads at an optimal speed. The distance between nodes is the optimal distance to keep the membrane still depolarized above threshold at the next node.
If the nodes were any closer together, the speed of propagation would be slower. Propagation along an unmyelinated axon is referred to as continuous conduction ; along the length of a myelinated axon, it is saltatory conduction. Along with the myelination of the axon, the diameter of the axon can influence the speed of conduction.
This concept is known as resistance and is generally true for electrical wires or plumbing, just as it is true for axons, although the specific conditions are different at the scales of electrons or ions versus water in a river.
Once in the synaptic cleft, the neurotransmitter diffuses the short distance to the postsynaptic membrane of the next neuron and interacts with neurotransmitter receptors on the dendrites or cell body.
Receptors are specific for the neurotransmitter, and the two fit together like a key and lock. One neurotransmitter binds to its receptor and will not bind to receptors for other neurotransmitters, making the binding a specific chemical event Figure 8.
Glial cells, especially astrocytes, are responsible for maintaining the chemical environment of the CNS tissue. The concentrations of ions in the extracellular fluid are the basis for how the membrane potential is established and changes in electrochemical signaling.
If the balance of ions is upset, drastic outcomes are possible. But when the level is far out of balance, the effects can be irreversible. Astrocytes can become reactive in cases such as these, which impairs their ability to maintain the local chemical environment. The glial cells enlarge and their processes swell.
When that is lost, the cell cannot get the energy it needs. In the central nervous system, carbohydrate metabolism is the only means of producing ATP. Elsewhere in the body, cells rely on carbohydrates, lipids, or amino acids to power mitochondrial ATP production. But the CNS does not store lipids in adipocytes fat cells as an energy reserve. The lipids in the CNS are in the cell membranes of neurons and glial cells, notably as an integral component of myelin.
Proteins in the CNS are crucial to neuronal function, in roles such as channels for electrical signaling or as part of the cytoskeleton. Those macromolecules are not used to power mitochondrial ATP production in neurons. For proteins to function correctly, they are dependent on their three-dimensional shape.
The linear sequence of amino acids folds into a three-dimensional shape that is based on the interactions between and among those amino acids. When the folding is disturbed, and proteins take on a different shape, they stop functioning correctly.
But the disease is not necessarily the result of functional loss of these proteins; rather, these altered proteins start to accumulate and may become toxic. Diseases of other organ systems can fall into this group as well, such as cystic fibrosis or type 2 diabetes. Recognizing the relationship between these diseases has suggested new therapeutic possibilities. Interfering with the accumulation of the proteins, and possibly as early as their original production within the cell, may unlock new ways to alleviate these devastating diseases.
Visit this site to see a virtual neurophysiology lab, and to observe electrophysiological processes in the nervous system, where scientists directly measure the electrical signals produced by neurons.
Often, the action potentials occur so rapidly that watching a screen to see them occur is not helpful. These action potentials are firing so fast that it sounds like static on the radio. Electrophysiologists can recognize the patterns within that static to understand what is happening. Why is the leech model used for measuring the electrical activity of neurons instead of using humans?
Skip to main content. Chapter 8: The Nervous System. Search for:. Impulse Conduction Learning Objectives Distinguish the major functions of the nervous system: sensation, integration, and response Describe the components of the membrane that establish the resting membrane potential Describe the changes that occur to the membrane that result in the action potential applying the terms polarized, depolarized, and repolarized.
Describe the process of propagation in a myelinated neuron and an unmyelinated neuron. Explain how neurotransmitters are used in neuron communication. For example, during the development of PNS myelinated nerve fibers, a molecule called gliomedin is secreted from myelinating Schwann cells then incorporated into the extracellular matrix surrounding nodes, where it promotes assembly of nodal axonal molecules. Due to the presence of the insulating myelin sheath at internodes and voltage-gated sodium channels at nodes, the action potential in myelinated nerve fibers jumps from one node to the next.
This mode of travel by the action potential is called "saltatory conduction" and allows for rapid impulse propagation Figure 1A. Following demyelination, a demyelinated axon has two possible fates. The normal response to demyelination, at least in most experimental models, is spontaneous remyelination involving the generation of new oligodendrocytes.
In some circumstances, remyelination fails, leaving the axons and even the entire neuron vulnerable to degeneration. Remyelination in the CNS: from biology to therapy. Nature Reviews Neuroscience 9, — All rights reserved. Figure Detail What happens if myelin is damaged? The importance of myelin is underscored by the presence of various diseases in which the primary problem is defective myelination. Demyelination is the condition in which preexisting myelin sheaths are damaged and subsequently lost, and it is one of the leading causes of neurological disease Figure 2.
Primary demyelination can be induced by several mechanisms, including inflammatory or metabolic causes. Myelin defects also occur by genetic abnormalities that affect glial cells. Regardless of its cause, myelin loss causes remarkable nerve dysfunction because nerve conduction can be slowed or blocked, resulting in the damaged information networks between the brain and the body or within the brain itself Figure 3.
Following demyelination, the naked axon can be re-covered by new myelin. This process is called remyelination and is associated with functional recovery Franklin and ffrench-Constant The myelin sheaths generated during remyelination are typically thinner and shorter than those generated during developmental myelination.
In some circumstances, however, remyelination fails, leaving axons and even the entire neuron vulnerable to degeneration. Thus, patients with demyelinating diseases suffer from various neurological symptoms. The representative demyelinating disease , and perhaps the most well known, is multiple sclerosis MS. This autoimmune neurological disorder is caused by the spreading of demyelinating CNS lesions in the entire brain and over time Siffrin et al. Patients with MS develop various symptoms, including visual loss, cognitive dysfunction, motor weakness, and pain.
Approximately 80 percent of patients experience relapse and remitting episodes of neurologic deficits in the early phase of the disease relapse-remitting MS. There are no clinical deteriorations between two episodes. Approximately ten years after disease onset, about one-half of MS patients suffer from progressive neurological deterioration secondary progressive MS.
About 10—15 percent of patients never experience relapsing-remitting episodes; their neurological status deteriorates continuously without any improvement primary progressive MS. Importantly, the loss of axons and their neurons is a major factor determining long-term disability in patients, although the primary cause of the disease is demyelination. Several immunodulative therapies are in use to prevent new attacks; however, there is no known cure for MS.
Figure 3 Despite the severe outcome and considerable effect of demyelinating diseases on patients' lives and society, little is known about the mechanism by which myelin is disrupted, how axons degenerate after demyelination, or how remyelination can be facilitated.
To establish new treatments for demyelinating diseases, a better understanding of myelin biology and pathology is absolutely required. How do we structure a research effort to elucidate the mechanisms involved in developmental myelination and demyelinating diseases?
We need to develop useful models to test drugs or to modify molecular expression in glial cells. One strong strategy is to use a culture system. Coculture of dorsal root ganglion neurons and Schwann cells can promote efficient myelin formation in vitro Figure 1E. Researchers can modify the molecular expression in Schwann cells, neurons, or both by various methods, including drugs, enzymes, and introducing genes , and can observe the consequences in the culture dish.
Modeling demyelinating disease in laboratory animals is commonly accomplished by treatment with toxins injurious to glial cells such as lysolecithin or cuprizone. Autoimmune diseases such as MS or autoimmune neuropathies can be reproduced by sensitizing animals with myelin proteins or lipids Figure 3.
Some mutant animals with defects in myelin proteins and lipids have been discovered or generated, providing useful disease models for hereditary demyelinating disorders. Further research is required to understand myelin biology and pathology in detail and to establish new treatment strategies for demyelinating neurological disorders.
Myelin can greatly increase the speed of electrical impulses in neurons because it insulates the axon and assembles voltage-gated sodium channel clusters at discrete nodes along its length. Myelin damage causes several neurological diseases, such as multiple sclerosis.
Future studies for myelin biology and pathology will provide important clues for establishing new treatments for demyelinating diseases. Brinkmann, B. Neuron 59 , — Franklin, R. Remyelination in the CNS: From biology to therapy. Nature Reviews Neuroscience 9 , — Nave, K. Axonal regulation of myelination by neuregulin 1. Current Opinion in Neurobiology 16 , — Poliak, S. The local differentiation of myelinated axons at nodes of Ranvier.
Nature Reviews Neuroscience 4 , — Sherman, D. Mechanisms of axon ensheathment and myelin growth. Nature Reviews Neuroscience 6 , — Siffrin, V. Multiple sclerosis — candidate mechanisms underlying CNS atrophy. Trends in Neurosciences 33 , — Susuki, K. Molecular mechanisms of node of Ranvier formation. Current Opinion in Cell Biology 20 , — Cell Signaling. Ion Channel. Cell Adhesion and Cell Communication.
Aging and Cell Division. Endosomes in Plants. Ephs, Ephrins, and Bidirectional Signaling. Ion Channels and Excitable Cells. Signal Transduction by Adhesion Receptors. Citation: Susuki, K. Nature Education 3 9 How does our nervous system operate so quickly and efficiently?
The answer lies in a membranous structure called myelin. Aa Aa Aa. Information Transmission in the Body. Figure 1. Figure Detail.
Axonal Signaling Regulates Myelination. Figure 2: The fate of demyelinated axons. The case in the CNS is illustrated. Research in Myelin Biology and Pathology.
Figure 3. References and Recommended Reading Brinkmann, B. Waxman, S. The Axon: Structure, Function and Pathophysiology. New York: Oxford University Press, Article History Close. Share Cancel. Revoke Cancel.
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