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42.2: The Mechanism of Nerve Impulse Transmission

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Skills to Develop

Describe the basis of the resting membrane potential
Explain the stages of an action potential and how action potentials are propagated
Explain the similarities and differences between chemical and electrical synapses
Describe long-term potentiation and long-term depression

All functions performed by the nervous system—from a simple motor reflex to more advanced functions like making a memory or a decision—require neurons to communicate with one another. While humans use words and body language to communicate, neurons use electrical and chemical signals. Just like a person in a committee, one neuron usually receives and synthesizes messages from multiple other neurons before “making the decision” to send the message on to other neurons.

Nerve Impulse Transmission within a Neuron

For the nervous system to function, neurons must be able to send and receive signals. These signals are possible because each neuron has a charged cellular membrane (a voltage difference between the inside and the outside), and the charge of this membrane can change in response to neurotransmitter molecules released from other neurons and environmental stimuli. To understand how neurons communicate, one must first understand the basis of the baseline or ‘resting’ membrane charge.

Neuronal Charged Membranes

The lipid bilayer membrane that surrounds a neuron is impermeable to charged molecules or ions. To enter or exit the neuron, ions must pass through special proteins called ion channels that span the membrane. Ion channels have different configurations: open, closed, and inactive, as illustrated in Figure $\PageIndex{1}$. Some ion channels need to be activated in order to open and allow ions to pass into or out of the cell. These ion channels are sensitive to the environment and can change their shape accordingly. Ion channels that change their structure in response to voltage changes are called voltage-gated ion channels. Voltage-gated ion channels regulate the relative concentrations of different ions inside and outside the cell. The difference in total charge between the inside and outside of the cell is called the membrane potential .

The first image shows a voltage-gated sodium channel that is closed at the resting potential. In response to a nerve impulse the channel opens, allowing sodium to enter the cell. After the impulse the channel enters an inactive state. The channel closes by a different mechanism and, for a brief period does not reopen in response to a new nerve impulse.

Link to Learning

This video discusses the basis of the resting membrane potential.

Resting Membrane Potential

A neuron at rest is negatively charged: the inside of a cell is approximately 70 millivolts more negative than the outside (−70 mV, note that this number varies by neuron type and by species). This voltage is called the resting membrane potential; it is caused by differences in the concentrations of ions inside and outside the cell. If the membrane were equally permeable to all ions, each type of ion would flow across the membrane and the system would reach equilibrium. Because ions cannot simply cross the membrane at will, there are different concentrations of several ions inside and outside the cell, as shown in the table below. The difference in the number of positively charged potassium ions (K + ) inside and outside the cell dominates the resting membrane potential (Figure $\PageIndex{2}$). When the membrane is at rest, K + ions accumulate inside the cell due to a net movement with the concentration gradient. The negative resting membrane potential is created and maintained by increasing the concentration of cations outside the cell (in the extracellular fluid) relative to inside the cell (in the cytoplasm). The negative charge within the cell is created by the cell membrane being more permeable to potassium ion movement than sodium ion movement. In neurons, potassium ions are maintained at high concentrations within the cell while sodium ions are maintained at high concentrations outside of the cell. The cell possesses potassium and sodium leakage channels that allow the two cations to diffuse down their concentration gradient. However, the neurons have far more potassium leakage channels than sodium leakage channels. Therefore, potassium diffuses out of the cell at a much faster rate than sodium leaks in. Because more cations are leaving the cell than are entering, this causes the interior of the cell to be negatively charged relative to the outside of the cell. The actions of the sodium potassium pump help to maintain the resting potential, once established. Recall that sodium potassium pumps brings two K + ions into the cell while removing three Na + ions per ATP consumed. As more cations are expelled from the cell than taken in, the inside of the cell remains negatively charged relative to the extracellular fluid. It should be noted that calcium ions (Cl – ) tend to accumulate outside of the cell because they are repelled by negatively-charged proteins within the cytoplasm.

Action Potential

A neuron can receive input from other neurons and, if this input is strong enough, send the signal to downstream neurons. Transmission of a signal between neurons is generally carried by a chemical called a neurotransmitter. Transmission of a signal within a neuron (from dendrite to axon terminal) is carried by a brief reversal of the resting membrane potential called an action potential . When neurotransmitter molecules bind to receptors located on a neuron’s dendrites, ion channels open. At excitatory synapses, this opening allows positive ions to enter the neuron and results in depolarization of the membrane—a decrease in the difference in voltage between the inside and outside of the neuron. A stimulus from a sensory cell or another neuron depolarizes the target neuron to its threshold potential (-55 mV). Na + channels in the axon hillock open, allowing positive ions to enter the cell (Figure $\PageIndex{3}$ and Figure $\PageIndex{4}$). Once the sodium channels open, the neuron completely depolarizes to a membrane potential of about +40 mV. Action potentials are considered an "all-or nothing" event, in that, once the threshold potential is reached, the neuron always completely depolarizes. Once depolarization is complete, the cell must now "reset" its membrane voltage back to the resting potential. To accomplish this, the Na + channels close and cannot be opened. This begins the neuron's refractory period , in which it cannot produce another action potential because its sodium channels will not open. At the same time, voltage-gated K + channels open, allowing K + to leave the cell. As K + ions leave the cell, the membrane potential once again becomes negative. The diffusion of K + out of the cell actually hyperpolarizes the cell, in that the membrane potential becomes more negative than the cell's normal resting potential. At this point, the sodium channels will return to their resting state, meaning they are ready to open again if the membrane potential again exceeds the threshold potential. Eventually the extra K + ions diffuse out of the cell through the potassium leakage channels, bringing the cell from its hyperpolarized state, back to its resting membrane potential.

Art Connection

Graph plots membrane potential in millivolts versus time. The membrane remains at the resting potential of -70 millivolts until a nerve impulse occurs in step 1. Some sodium channels open, and the potential begins to rapidly climb past the threshold of excitation of -55 millivolts, at which point all the sodium channels open. At the peak action potential, the potential begins to rapidly drop as potassium channels open and sodium channels close. As a result, the membrane repolarizes past the resting membrane potential and becomes hyperpolarized. The membrane potential then gradually returns to normal.

Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, called cardiac dysrhythmia, impede the movement of K + through voltage-gated K + channels. Which part of the action potential would you expect potassium channels to affect?

The action potential travels from the soma down the axon to the axon terminal. The action potential is initiated when a signal from the soma causes the soma-end of the axon membrane to depolarize. The depolarization spreads down the axon. Meanwhile, the membrane at the start of the axon repolarizes. Because potassium channels are open, the membrane cannot depolarize again. The action potential continues to spread down the axon this way.

This video presents an overview of action potential.

Myelin and the Propagation of the Action Potential

For an action potential to communicate information to another neuron, it must travel along the axon and reach the axon terminals where it can initiate neurotransmitter release. The speed of conduction of an action potential along an axon is influenced by both the diameter of the axon and the axon’s resistance to current leak. Myelin acts as an insulator that prevents current from leaving the axon; this increases the speed of action potential conduction. In demyelinating diseases like multiple sclerosis, action potential conduction slows because current leaks from previously insulated axon areas. The nodes of Ranvier, illustrated in Figure $\PageIndex{5}$ are gaps in the myelin sheath along the axon. These unmyelinated spaces are about one micrometer long and contain voltage gated Na + and K + channels. Flow of ions through these channels, particularly the Na + channels, regenerates the action potential over and over again along the axon. This ‘jumping’ of the action potential from one node to the next is called saltatory conduction . If nodes of Ranvier were not present along an axon, the action potential would propagate very slowly since Na + and K + channels would have to continuously regenerate action potentials at every point along the axon instead of at specific points. Nodes of Ranvier also save energy for the neuron since the channels only need to be present at the nodes and not along the entire axon.

Illustration shows an axon covered in three bands of myelin sheath. Between the sheath coverings the axon is exposed. The uncovered parts of the axon are called nodes of Ranvier. In the illustration, the left node of Ranvier is depolarized such that the membrane potential is positive inside and negative outside. The right membrane of the right node is at the resting potential, negative inside and positive outside. An arrow indicates that the depolarization jumps from the left node to the right, so that the right node becomes depolarized.

Synaptic Transmission

The synapse or “gap” is the place where information is transmitted from one neuron to another. Synapses usually form between axon terminals and dendritic spines, but this is not universally true. There are also axon-to-axon, dendrite-to-dendrite, and axon-to-cell body synapses. The neuron transmitting the signal is called the presynaptic neuron, and the neuron receiving the signal is called the postsynaptic neuron. Note that these designations are relative to a particular synapse—most neurons are both presynaptic and postsynaptic. There are two types of synapses: chemical and electrical.

Chemical Synapse

When an action potential reaches the axon terminal it depolarizes the membrane and opens voltage-gated Na + channels. Na + ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated Ca 2+ channels to open. Calcium ions entering the cell initiate a signaling cascade that causes small membrane-bound vesicles, called synaptic vesicles , containing neurotransmitter molecules to fuse with the presynaptic membrane. Synaptic vesicles are shown in Figure $\PageIndex{6}$, which is an image from a scanning electron microscope.

The axon terminal is spherical. A section is sliced off, revealing small blue and orange vesicles just inside.

Fusion of a vesicle with the presynaptic membrane causes neurotransmitter to be released into the synaptic cleft , the extracellular space between the presynaptic and postsynaptic membranes, as illustrated in Figure $\PageIndex{7}$. The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane.

Illustration shows a narrow axon of a presynaptic cell widening into a bulb-like axon terminal. A narrow synaptic cleft separates the axon terminal of the presynaptic cell from the postsynaptic cell. In step 1, an action potential arrives at the axon terminal. In step 2, the action potential causes voltage-gated calcium channels in the axon terminal open, allowing calcium to enter. In step 3, calcium influx causes neurotransmitter-containing synaptic vesicles to fuse with the plasma membrane. Contents of the vesicles are released into the synaptic cleft by exocytosis. In step 4, neurotransmitter diffuses across the synaptic cleft and binds ligand-gated ion channels on the postsynaptic membrane, causing the channels to open. In step 5, the open channels cause ion movement into or out of the cell, resulting in a localized change in membrane potential. In step 6, reuptake by the presynaptic neuron, enzymatic degradation and diffusion reduce neurotransmitter levels, terminating the signal.

The binding of a specific neurotransmitter causes particular ion channels, in this case ligand-gated channels, on the postsynaptic membrane to open. Neurotransmitters can either have excitatory or inhibitory effects on the postsynaptic membrane, as detailed in the table below. For example, when acetylcholine is released at the synapse between a nerve and muscle (called the neuromuscular junction) by a presynaptic neuron, it causes postsynaptic Na + channels to open. Na + enters the postsynaptic cell and causes the postsynaptic membrane to depolarize. This depolarization is called an excitatory postsynaptic potential (EPSP) and makes the postsynaptic neuron more likely to fire an action potential. Release of neurotransmitter at inhibitory synapses causes inhibitory postsynaptic potentials (IPSPs) , a hyperpolarization of the presynaptic membrane. For example, when the neurotransmitter GABA (gamma-aminobutyric acid) is released from a presynaptic neuron, it binds to and opens Cl - channels. Cl - ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire an action potential.

Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. This can be accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be degraded by enzymes in the synaptic cleft, or it can be recycled (sometimes called reuptake) by the presynaptic neuron. Several drugs act at this step of neurotransmission. For example, some drugs that are given to Alzheimer’s patients work by inhibiting acetylcholinesterase, the enzyme that degrades acetylcholine. This inhibition of the enzyme essentially increases neurotransmission at synapses that release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and unbind to postsynaptic receptors.

Electrical Synapse

While electrical synapses are fewer in number than chemical synapses, they are found in all nervous systems and play important and unique roles. The mode of neurotransmission in electrical synapses is quite different from that in chemical synapses. In an electrical synapse, the presynaptic and postsynaptic membranes are very close together and are actually physically connected by channel proteins forming gap junctions. Gap junctions allow current to pass directly from one cell to the next. In addition to the ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction pores.

There are key differences between chemical and electrical synapses. Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is unidirectional. Signaling in electrical synapses, in contrast, is virtually instantaneous (which is important for synapses involved in key reflexes), and some electrical synapses are bidirectional. Electrical synapses are also more reliable as they are less likely to be blocked, and they are important for synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures.

Signal Summation

Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron, but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential. This process is called summation and occurs at the axon hillock, as illustrated in Figure $\PageIndex{8}$. Additionally, one neuron often has inputs from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPs and vice versa. It is the net change in postsynaptic membrane voltage that determines whether the postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together, synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system is not transmitted as important information.

Illustration shows the location of the axon hillock, which is the area connecting the neuron body to the axon. A graph shows the summation of membrane potentials at the axon hillock, plotted as membrane potential in millivolts versus time. Initially, the membrane potential at the axon hillock is -70 millivolts. A series of EPSPs and IPSPs cause the potential to rise and fall. Eventually, the potential increases to the threshold of excitation. At this point the nerve fires, resulting in a sharp increase in membrane potential, followed by a rapid decrease. The hillock becomes hyperpolarizes such that the membrane potential is lower than the resting potential. The hillock then gradually returns to the resting potential.

Everyday Connection: Brain-computer interface

Amyotrophic lateral sclerosis (ALS, also called Lou Gehrig’s Disease) is a neurological disease characterized by the degeneration of the motor neurons that control voluntary movements. The disease begins with muscle weakening and lack of coordination and eventually destroys the neurons that control speech, breathing, and swallowing; in the end, the disease can lead to paralysis. At that point, patients require assistance from machines to be able to breathe and to communicate. Several special technologies have been developed to allow “locked-in” patients to communicate with the rest of the world. One technology, for example, allows patients to type out sentences by twitching their cheek. These sentences can then be read aloud by a computer.

A relatively new line of research for helping paralyzed patients, including those with ALS, to communicate and retain a degree of self-sufficiency is called brain-computer interface (BCI) technology and is illustrated in Figure $\PageIndex{9}$. This technology sounds like something out of science fiction: it allows paralyzed patients to control a computer using only their thoughts. There are several forms of BCI. Some forms use EEG recordings from electrodes taped onto the skull. These recordings contain information from large populations of neurons that can be decoded by a computer. Other forms of BCI require the implantation of an array of electrodes smaller than a postage stamp in the arm and hand area of the motor cortex. This form of BCI, while more invasive, is very powerful as each electrode can record actual action potentials from one or more neurons. These signals are then sent to a computer, which has been trained to decode the signal and feed it to a tool—such as a cursor on a computer screen. This means that a patient with ALS can use e-mail, read the Internet, and communicate with others by thinking of moving his or her hand or arm (even though the paralyzed patient cannot make that bodily movement). Recent advances have allowed a paralyzed locked-in patient who suffered a stroke 15 years ago to control a robotic arm and even to feed herself coffee using BCI technology.

Despite the amazing advancements in BCI technology, it also has limitations. The technology can require many hours of training and long periods of intense concentration for the patient; it can also require brain surgery to implant the devices.

Illustration shows a person in a wheelchair, facing a computer screen. An arrow indicates that neural signals travel from the brain of the paralyzed person to the computer.

Watch this video in which a paralyzed woman use a brain-controlled robotic arm to bring a drink to her mouth, among other images of brain-computer interface technology in action.

Synaptic Plasticity

Synapses are not static structures. They can be weakened or strengthened. They can be broken, and new synapses can be made. Synaptic plasticity allows for these changes, which are all needed for a functioning nervous system. In fact, synaptic plasticity is the basis of learning and memory. Two processes in particular, long-term potentiation (LTP) and long-term depression (LTD) are important forms of synaptic plasticity that occur in synapses in the hippocampus, a brain region that is involved in storing memories.

Long-term Potentiation (LTP)

Long-term potentiation (LTP) is a persistent strengthening of a synaptic connection. LTP is based on the Hebbian principle: cells that fire together wire together. There are various mechanisms, none fully understood, behind the synaptic strengthening seen with LTP. One known mechanism involves a type of postsynaptic glutamate receptor, called NMDA (N-Methyl-D-aspartate) receptors, shown in Figure $\PageIndex{10}$. These receptors are normally blocked by magnesium ions; however, when the postsynaptic neuron is depolarized by multiple presynaptic inputs in quick succession (either from one neuron or multiple neurons), the magnesium ions are forced out allowing Ca ions to pass into the postsynaptic cell. Next, Ca 2+ ions entering the cell initiate a signaling cascade that causes a different type of glutamate receptor, called AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors, to be inserted into the postsynaptic membrane, since activated AMPA receptors allow positive ions to enter the cell. So, the next time glutamate is released from the presynaptic membrane, it will have a larger excitatory effect (EPSP) on the postsynaptic cell because the binding of glutamate to these AMPA receptors will allow more positive ions into the cell. The insertion of additional AMPA receptors strengthens the synapse and means that the postsynaptic neuron is more likely to fire in response to presynaptic neurotransmitter release. Some drugs of abuse co-opt the LTP pathway, and this synaptic strengthening can lead to addiction.

Long-term Depression (LTD)

Long-term depression (LTD) is essentially the reverse of LTP: it is a long-term weakening of a synaptic connection. One mechanism known to cause LTD also involves AMPA receptors. In this situation, calcium that enters through NMDA receptors initiates a different signaling cascade, which results in the removal of AMPA receptors from the postsynaptic membrane, as illustrated in Figure $\PageIndex{10}$. The decrease in AMPA receptors in the membrane makes the postsynaptic neuron less responsive to glutamate released from the presynaptic neuron. While it may seem counterintuitive, LTD may be just as important for learning and memory as LTP. The weakening and pruning of unused synapses allows for unimportant connections to be lost and makes the synapses that have undergone LTP that much stronger by comparison.

Illustration shows the mechanism of LTP and LTD. Normally, the NMDA receptor in the postsynaptic neuron is activated by glutamate binding, but only after depolarization removes an inhibitory magnesium ion. Once the magnesium is removed, calcium can enter the cell. In response to an increase in intracellular calcium, AMPA receptors are inserted into the plasma membrane, which amplifies the signal resulting in LTP. LDP occurs when low-frequency stimulation results in the activation of a different calcium-signaling cascade that causes AMPA receptors to be removed from the plasma membrane. As a result, the nerve cell becomes less responsive to glutamate.

Neurons have charged membranes because there are different concentrations of ions inside and outside of the cell. Voltage-gated ion channels control the movement of ions into and out of a neuron. When a neuronal membrane is depolarized to at least the threshold of excitation, an action potential is fired. The action potential is then propagated along a myelinated axon to the axon terminals. In a chemical synapse, the action potential causes release of neurotransmitter molecules into the synaptic cleft. Through binding to postsynaptic receptors, the neurotransmitter can cause excitatory or inhibitory postsynaptic potentials by depolarizing or hyperpolarizing, respectively, the postsynaptic membrane. In electrical synapses, the action potential is directly communicated to the postsynaptic cell through gap junctions—large channel proteins that connect the pre-and postsynaptic membranes. Synapses are not static structures and can be strengthened and weakened. Two mechanisms of synaptic plasticity are long-term potentiation and long-term depression.

Art Connections

Figure $\PageIndex{3}$: Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, called cardiac dysrhythmia, impede the movement of K + through voltage-gated K + channels. Which part of the action potential would you expect potassium channels to affect?

Potassium channel blockers slow the repolarization phase, but have no effect on depolarization.

It feels instantaneous, but how long does it really take to think a thought?

Professor of Kinesiology and Physical Education, University of Toronto

Disclosure statement

Tim Welsh receives funding from Natural Sciences and Engineering Research Council of Canada.

University of Toronto provides funding as a founding partner of The Conversation CA.

University of Toronto provides funding as a member of The Conversation CA-FR.

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As inquisitive beings, we are constantly questioning and quantifying the speed of various things. With a fair degree of accuracy, scientists have quantified the speed of light, the speed of sound , the speed at which the earth revolves around the sun , the speed at which hummingbirds beat their wings , the average speed of continental drift ….

These values are all well-characterized. But what about the speed of thought? It’s a challenging question that’s not easily answerable – but we can give it a shot.

First, some thoughts on thought

To quantify the speed of anything, one needs to identify its beginning and end. For our purposes, a “thought” will be defined as the mental activities engaged from the moment sensory information is received to the moment an action is initiated. This definition necessarily excludes many experiences and processes one might consider to be “thoughts.”

Here, a “thought” includes processes related to perception (determining what is in the environment and where), decision-making (determining what to do) and action-planning (determining how to do it). The distinction between, and independence of, each of these processes is blurry. Further, each of these processes, and perhaps even their sub-components, could be considered “thoughts” on their own. But we have to set our start- and endpoints somewhere to have any hope of tackling the question.

Finally, trying to identify one value for the “speed of thought” is a little like trying to identify one maximum speed for all forms of transportation, from bicycles to rockets. There are many different kinds of thoughts that can vary greatly in timescale. Consider the differences between simple, speedy reactions like the sprinter deciding to run after the crack of the starting pistol (on the order of 150 milliseconds [ms]), and more complex decisions like deciding when to change lanes while driving on a highway or figuring out the appropriate strategy to solve a math problem (on the order of seconds to minutes).

Thoughts are invisible, so what should we measure?

Thought is ultimately an internal and very individualized process that’s not readily observable. It relies on interactions across complex networks of neurons distributed throughout the peripheral and central nervous systems. Researchers can use imaging techniques, such as functional magnetic resonance imaging and electroencephalography , to see what areas of the nervous system are active during different thought processes, and how information flows through the nervous system. We’re still a long way from reliably relating these signals to the mental events they represent, though.

Many scientists consider the best proxy measure of the speed or efficiency of thought processes to be reaction time – the time from the onset of a specific signal to the moment an action is initiated. Indeed, researchers interested in assessing how fast information travels through the nervous system have used reaction time since the mid-1800s . This approach makes sense because thoughts are ultimately expressed through overt actions. Reaction time provides an index of how efficiently someone receives and interprets sensory information, decides what to do based on that information, and plans and initiates an action based on that decision.

Neural factors involved

The time it takes for all thoughts to occur is ultimately shaped by the characteristics of the neurons and the networks involved. Many things influence the speed at which information flows through the system, but three key factors are:

Distance – The farther signals need to travel, the longer the reaction time is going to be. Reaction times for movements of the foot are longer than for movements of the hand, in large part because the signals traveling to and from the brain have a longer distance to cover. This principle is readily demonstrated through reflexes (note, however, that reflexes are responses that occur without “thought” because they do not involve neurons that engaged in conscious thought). The key observation for the present purpose is that the same reflexes evoked in taller individuals tend to have longer response times than for shorter individuals. By way of analogy, if two couriers driving to New York leave at the same time and travel at exactly the same speed, a courier leaving from Washington, DC will always arrive before one leaving from Los Angeles.

Neuron characteristics – The width of the neuron is important. Signals are carried more quickly in neurons with larger diameters than those that are narrower – a courier will generally travel faster on wide multi-lane highways than on narrow country roads.

How much myelination a neuron has is also important. Some nerve cells have myelin cells that wrap around the neuron to provide a type of insulation sheath. The myelin sheath isn’t completely continuous along a neuron; there are small gaps in which the nerve cell is exposed. Nerve signals effectively jump from exposed section to exposed section instead of traveling the full extent of the neuronal surface. So signals move much faster in neurons that have myelin sheaths than in neurons that don’t. The message will get to New York sooner if it passes from cellphone tower to cellphone tower than if the courier drives the message along each and every inch of the road. In the human context, the signals carried by the large-diameter, myelinated neurons that link the spinal cord to the muscles can travel at speeds ranging from 70-120 meters per second (m/s) (156-270 miles per hour[mph]), while signals traveling along the same paths carried by the small-diameter, unmyelinated fibers of the pain receptors travel at speeds ranging from 0.5-2 m/s (1.1-4.4 mph). That’s quite a difference!

Complexity – Increasing the number of neurons involved in a thought means a greater absolute distance the signal needs to travel – which necessarily means more time. The courier from Washington, DC will take less time to get to New York with a direct route than if she travels to Chicago and Boston along the way. Further, more neurons mean more connections. Most neurons are not in physical contact with other neurons. Instead, most signals are passed via neurotransmitter molecules that travel across the small spaces between the nerve cells called synapses. This process takes more time (at least 0.5 ms per synapse) than if the signal was continually passed within the single neuron. The message carried from Washington, DC will take less time to get to New York if one single courier does the whole route than if multiple couriers are involved, stopping and handing over the message several times along the way. In truth, even the “simplest” thoughts involve multiple structures and hundreds of thousands of neurons.

How quickly it can happen

It’s amazing to consider that a given thought can be generated and acted on in less than 150 ms. Consider the sprinter at a starting line. The reception and perception of the crack of the starter’s gun, the decision to begin running, issuing of the movement commands, and generating muscle force to start running involves a network that begins in the inner ear and travels through numerous structures of the nervous system before reaching the muscles of the legs. All that can happen in literally half the time of a blink of an eye.

Although the time to initiate a sprint start is extremely short, a variety of factors can influence it. One is the loudness of the auditory “go” signal . Although reaction time tends to decrease as the loudness of the “go” increases, there appears to be a critical point in the range of 120-124 decibels where an additional decrease of approximately 18 ms can occur. That’s because sounds this loud can generate the “startle” response and trigger a pre-planned sprinting response.

Researchers think this triggered response emerges through activation of neural centers in the brain stem . These startle-elicited responses may be quicker because they involve a relatively shorter and less complex neural system – one that does not necessarily require the signal to travel all the way up to the more complex structures of the cerebral cortex. A debate could be had here as to whether or not these triggered responses are “thoughts,” because it can be questioned whether or not a true decision to act was made; but the reaction time differences of these responses illustrate the effect of neural factors such as distance and complexity. Involuntary reflexes, too, involve shorter and simpler circuitry and tend to take less time to execute than voluntary responses.

Perceptions of our thoughts and actions

Considering how quickly they do happen, it’s little wonder we often feel our thoughts and actions are nearly instantaneous. But it turns out we’re also poor judges of when our actions actually occur.

Although we’re aware of our thoughts and the resulting movements, an interesting dissociation has been observed between the time we think we initiate a movement and when that movement actually starts . In studies, researchers ask volunteers to watch a second hand rotate around a clock face and to complete a simple rapid finger or wrist movement, such as a key press, whenever they liked. After the clock hand had completed its rotation, the people were asked to identify where the hand was on the clock face when they started their own movement.

Surprisingly, people typically judge the onset of their movement to occur 75-100 ms prior to when it actually began. This difference cannot be accounted for simply by the time it takes for the movement commands to travel from the brain to the arm muscles (which is on the order of 16-25 ms). It’s unclear exactly why this misperception occurs, but it’s generally believed that people base their judgment of movement onset on the time of the decision to act and the prediction of the upcoming movement, instead of on the movement itself. These and other findings raise important questions about the planning and control of action and our sense of agency and control in the world – because our decision to act and our perception of when we act appear to be distinct from when we in fact do.

In sum, although quantifying a single “speed of thought” may never be possible, analyzing the time it takes to plan and complete actions provides important insights into how efficiently the nervous system completes these processes, and how changes associated with movement and cognitive disorders affect the efficiency of these mental activities.

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We take a closer look at the anatomy of the neuron and the role myelin plays in the rapid transmission of messages between brain cells.

In the neuron, a protective covering called myelin (grey) insulates the axon and increases the speed of electrical communication along the length of the neuron. Image: Opus Design

How do neurons communicate (so quickly)?

by Sabbi Lall | February 28, 2019 May 24, 2023

Categories: Cellular & Molecular Neuroscience , Guoping Feng , Ask the Brain

Neurons are the most fundamental unit of the nervous system, and yet, researchers are just beginning to understand how they perform the complex computations that underlie our behavior. We asked Boaz Barak , previously a postdoc in Guoping Feng ’s lab at the McGovern Institute and now Senior Lecturer at the School of Psychological Sciences and Sagol School of Neuroscience at Tel Aviv University, to unpack the basics of neuron communication for us.

“Neurons communicate with each other through electrical and chemical signals,” explains Barak. “The electrical signal, or action potential, runs from the cell body area to the axon terminals, through a thin fiber called axon. Some of these axons can be very long and most of them are very short. The electrical signal that runs along the axon is based on ion movement. The speed of the signal transmission is influenced by an insulating layer called myelin,” he explains.

Myelin is a fatty layer formed, in the vertebrate central nervous system, by concentric wrapping of oligodendrocyte cell processes around axons. The term “myelin” was coined in 1854 by Virchow (whose penchant for Greek and for naming new structures also led to the terms amyloid, leukemia, and chromatin). In more modern images, the myelin sheath is beautifully visible as concentric spirals surrounding the “tube” of the axon itself. Neurons in the peripheral nervous system are also myelinated, but the cells responsible for myelination are Schwann cells, rather than oligodendrocytes.

“Neurons communicate with each other through electrical and chemical signals,” explains Boaz Barak.

“Myelin’s main purpose is to insulate the neuron’s axon,” Barak says. “It speeds up conductivity and the transmission of electrical impulses. Myelin promotes fast transmission of electrical signals mainly by affecting two factors: 1) increasing electrical resistance, or reducing leakage of the electrical signal and ions along the axon, “trapping” them inside the axon and 2) decreasing membrane capacitance by increasing the distance between conducting materials inside the axon (intracellular fluids) and outside of it (extracellular fluids).”

Adjacent sections of axon in a given neuron are each surrounded by a distinct myelin sheath. Unmyelinated gaps between adjacent ensheathed regions of the axon are called Nodes of Ranvier, and are critical to fast transmission of action potentials, in what is termed “saltatory conduction.” A useful analogy is that if the axon itself is like an electrical wire, myelin is like insulation that surrounds it, speeding up impulse propagation, and overcoming the decrease in action potential size that would occur during transmission along a naked axon due to electrical signal leakage, how the myelin sheath promotes fast transmission that allows neurons to transmit information long distances in a timely fashion in the vertebrate nervous system.

Myelin seems to be critical to healthy functioning of the nervous system; in fact, disruptions in the myelin sheath have been linked to a variety of disorders.

“Abnormal myelination can arise from abnormal development caused by genetic alterations,” Barak explains further. “Demyelination can even occur, due to an autoimmune response, trauma, and other causes. In neurological conditions in which myelin properties are abnormal, as in the case of lesions or plaques, signal transmission can be affected. For example, defects in myelin can lead to lack of neuronal communication, as there may be a delay or reduction in transmission of electrical and chemical signals. Also, in cases of abnormal myelination, it is possible that the synchronicity of brain region activity might be affected, for example, leading to improper actions and behaviors.”

Researchers are still working to fully understand the role of myelin in disorders. Myelin has a long history of being evasive though, with its origins in the central nervous system being unclear for many years. For a period of time, the origin of myelin was thought to be the axon itself, and it was only after initial discovery (by Robertson, 1899), re-discovery (Del Rio-Hortega, 1919), and skepticism followed by eventual confirmation, that the role of oligodendrocytes in forming myelin became clear. With modern imaging and genetic tools, we should be able to increasingly understand its role in the healthy, as well as a compromised, nervous system.

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Nerve Impulses: the Key to Understanding the Brain

Impulses are the basis of mind..

Posted October 17, 2019

One of the greatest, relatively underappreciated, discoveries in all of science was the discovery of the nerve impulse in the 1930s by the British Lord Adrian. Adrian did win a Nobel Prize for his discovery in 1932, but scholars underestimated its implications, which go beyond the fact that four later Nobel Prizes were awarded for work based on Adrian’s discovery. This included discovery of sodium and potassium ionic flux during impulses, the role of impulses in releasing neurotransmitters, and the role of membrane ion channels in impulse generation and second messenger cascades.

Like many discoveries in science, this one could not have been made without technological advances. Early studies with inferior technology had a very poor signal-to-noise ratio (not the thick baseline electrical noise in the illustration). Vast improvements in this ratio are obtained with today's technology and intracellular recording. In Adrian's day, the essential advance was the development of the capillary electrometer, which enabled the detection of very small electrical pulses on the order of one-millisecond duration. This instrumentation was crude and far inferior to later advances such as the oscilloscope and computer screens. Before Adrian’s use of the electrometer, scientists generally knew that peripheral nerves generated some kind of electrical signal, but nothing was known about the nature of the signal in individual neurons.

Nerves contain fibers from hundreds of neurons that produce a summed, relatively long duration and large wave that spreads down the nerve. No one knew how the individual nerve fibers contributed to this compound signal. Adrian answered this question by tedious microdissection of nerves into their individual fibers and recording stimulus-evoked responses in a single fiber. What Adrian saw was that the response was a series of voltage pulses, each about one millisecond long, all of the same amplitude in a given fiber. Decades later, the development of microelectrodes enabled confirmation of Adrian’s discovery in neurons in the brain.

This provided evidence of the basic similarity and difference between brains and the later development of computers. Both computers and brains convert the real world into representations. In computers, information is coded, in the form of 1s and 0s, and as nerve impulses in brains. Both computers and brains distribute and process this represented information, and can store it as memories. However, because brains are biological and use impulses to represent information, they can change their circuitry and can self-program. Unlike computers, brains also have will, including a likely degree of free will .

Brains have conspicuous functional states, ranging from intense conscious concentration to drowsiness, to sleep, to coma, to death. Neuronal electrical activity correlates in a systematic way with these state changes. The most conspicuous of these activity measures exist in terms of nerve impulse firing and the extracellular ionic currents they create at synapses, known as field potentials. As these field potentials reach the scalp, they produce the signal we call an electroencephalogram. Field potentials are technologically easier to record than individual nerve impulses, but more ambiguous to interpret because of the spatial summation of voltages from hundreds of heterogeneous neurons.

The original nerve impulse findings were that the rate of impulse firing governed the impact on neuronal targets, whether they be muscle or other neurons. Various labs, including my own, in the 1980s, discovered that the intervals between impulses also contained their own kind of information. For example, my lab reported that some neurons contained statistically significant serial ordering of impulse intervals in a neuron’s impulse stream. The intervals, at least in higher-level brain areas, are not random. They are serially dependent, as if they contained a message. If you are familiar with Markov transition probability, you can understand our finding that serial dependences exist in as many as five successive intervals (Sherry et al. 1982). This led us to suggest “byte processing” as a basic feature of neuronal information processing. This view has not caught on, and most people still seem to think that firing rate is the basic information code, despite the well-established temporal summation that occurs as impulses arrive at synapses. Bernard Katz demonstrated temporal summation of impulse effects in neuromuscular junctions in 1951 and later J.P. Segundo and colleagues confirmed it in neuronal synapses (Segundo et al., 1963).

It should not be surprising that there are serial dependencies in impulse intervals. For example, intracellular recording of postsynaptic potentials revealed that the polarization change caused by a single impulse input decays in a few milliseconds. However, a succession of closely spaced impulse inputs allows the polarization changes to summate.

These days, the emphasis needs to be put on impulse activity in defined circuitry. All neurons are linked in one or more circuits, and the impulse train in any one neuron is only a small part of the over-all circuit activity. The function of any given circuit depends on the circuit impulse pattern (CIP) of the whole circuit. Researchers have developed microelectrodes that allow recording of impulse trains from single neurons, but the problem is in implanting a series of electrodes so that each one monitors the activity of a selected neuron in a defined.

I think that research should focus on CIPs and the phase relationships of electrical activity among cortical circuits, both within and among cortical columns (Klemm, 2011). Nerve impulses have to be at the heart of consciousness, inasmuch as impulses contain the brain’s representation of information and create the synaptic field potentials.

We know from monitoring known anatomical pathways for specific sensations that the brain creates a CIP representation of the stimuli. As long as the CIPs remain active, the representation of sensation or neural processing is intact and may even be accessible to consciousness. However, if something disrupts ongoing CIPs to create a different set of CIPs, as for example would happen with a different stimulus, then the original representation disappears. If the original CIPs persist long enough, a memory could form, but otherwise, the information would be lost. The implication for memory formation is that the immediate period after learning must be protected from new inputs to keep the CIP representation of the learning intact long enough to form a more lasting memory.

Much current research shows that conscious awareness correlates with the degree of synchrony and time-locking of CIPs in various regions and within regions of cortex. The evidence comes from electroencephalographic monitoring of the oscillating field potentials in a given area. These are voltage waves that occur in multiple frequency bands. Phase relationships of voltage waves from different circuits surely reflect the timing of the impulse discharges that create those fields. I summarized the animal research evidence for this view in my first book, some 50 years ago (Klemm, 1969). Depending on the nature of the stimulus and mental state, these oscillations of various circuits may jitter with respect to each other or become time locked. The functional consequence of synchrony has to be substantial, and many others and I suggest that this is a fundamental aspect of consciousness. The correlation between frequency coherences and states of consciousness is clear. Frequency coherence reflects a “binding” of neurons into linked and shared electrochemical activity, but how this relates to conscious awareness will require a next great discovery in science.

Klemm, W. R. (1969). Animal Electroencephalography. New York: Academic Press.

Klemm, W. R. (2011). Atoms of Mind. The “Ghost in the Machine” Materializes. New York: Springer.

Segundo, J. P., et al. (1963). Sensitivity of neurons in Aplysia to temporal pattern of arriving impulses. J. Exp. Biol. 40: 643-667.

Sherry, C. J., Barrow, D. L., and Klemm, W. R. 1982. Serial dependencies and Markov processes of neuronal interspike intervals from rat cerebellum. Brain Res. Bull. 8: 163‑169.

William Klemm , Ph.D ., is a senior professor of Neuroscience at Texas A&M University.

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11.41: Nerve Impulse

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What do nerve cells look like?

Note that like most other cells , these nerve cells have a nucleus . They also have other organelles . However, the long, threadlike extensions of the nerve cells are unique. This is where the nerve impulses are transmitted.

Neurons and Nerve Impulses

The nervous system is made up of nerves. A nerve is a bundle of nerve cells . A nerve cell that carries messages is called a neuron (Figure below). The messages carried by neurons are called nerve impulses . Nerve impulses can travel very quickly because they are electrical impulses.

Think about flipping on a light switch when you enter a room. When you flip the switch, the electricity flows to the light through wires inside the walls. The electricity may have to travel many meters to reach the light, but the light still comes on as soon as you flip the switch. Nerve impulses travel just as fast through the network of nerves inside the body.

What Does a Neuron Look Like?

A neuron has a special shape that lets it pass signals from one cell to another. A neuron has three main parts (Figure above):

The cell body.
Many dendrites.

The cell body contains the nucleus and other organelles . Dendrites and axons connect to the cell body, similar to rays coming off of the sun . Dendrites receive nerve impulses from other cells. Axons pass the nerve impulses on to other cells. A single neuron may have thousands of dendrites, so it can communicate with thousands of other cells but only one axon. The axon is covered with a myelin sheath , a fatty layer that insulates the axon and allows the electrical signal to travel much more quickly. The node of Ranvier is any gap within the myelin sheath exposing the axon, and it allows even faster transmission of a signal.

Types of Neurons

Neurons are usually classified based on the role they play in the body. Two main types of neurons are sensory neurons and motor neurons.

Sensory neurons carry nerve impulses from sense organs and internal organs to the central nervous system .
Motor neurons carry nerve impulses from the central nervous system to organs, glands, and muscles—the opposite direction.

Both types of neurons work together. Sensory neurons carry information about the environment found inside or outside of the body to the central nervous system . The central nervous system uses the information to send messages through motor neurons to tell the body how to respond to the information.

The Synapse

The place where the axon of one neuron meets the dendrite of another is called a synapse . Synapses are also found between neurons and other types of cells, such as muscle cells. The axon of the sending neuron does not actually touch the dendrite of the receiving neuron. There is a tiny gap between them, the synaptic cleft (Figure below).

The following steps describe what happens when a nerve impulse reaches the end of an axon.

When a nerve impulse reaches the end of an axon, the axon releases chemicals called neurotransmitters .
Neurotransmitters travel across the synapse between the axon and the dendrite of the next neuron.
Neurotransmitters bind to the membrane of the dendrite.
The binding allows the nerve impulse to travel through the receiving neuron.

Did you ever watch a relay race? After the first runner races, he or she passes the baton to the next runner, who takes over. Neurons are a little like relay runners. Instead of a baton, they pass neurotransmitters to the next neuron. Examples of neurotransmitters are chemicals such as serotonin, dopamine, and adrenaline.

You can watch an animation of nerve impulses and neurotransmitters at http://www.mind.ilstu.edu/curriculum/neurons_intro/neurons_intro.php .

Some people have low levels of the neurotransmitter called serotonin in their brain. Scientists think that this is one cause of depression. Medications called antidepressants help bring serotonin levels back to normal. For many people with depression, antidepressants control the symptoms of their depression and help them lead happy, productive lives.

Neurons, or nerve cells that carry nerve impulses, are made up of the cell body, the axon, and several dendrites.
Signals move across the synapse, the place where the axon of one neuron meets the dendrite of another, using chemicals called neurotransmitters.

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Use the resource below to answer the questions that follow.

Neuroscience For Kids at http://faculty.washington.edu/chudler/cells.html
What are the three types of neurons?
What neurons are most abundant in the central nervous system?
What is the function of sensory neurons?
What is the function of motor neurons?
What is the role of interneurons?
Describe a neuron and identify its three main parts.
Distinguish between dendrites and the axon.
Distinguish between sensory and motor neurons.
Explain how one neuron transmits a nerve impulse to another neuron.

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Numbers: The Nervous System, From 268-MPH Signals to Trillions of Synapses

268 Speed (in miles per hour) at which signals travel along an alpha motor neuron in the spinal cord, the fastest such transmission in the human body. Sensory receptors in the skin, which lack the speed-boosting insulating layer called a myelin sheath, are among the slowest, at 1 mph.

100,000 Miles of myelin-covered nerve fibers in the brain of an average 20-year-old. Neuroscientists at UCLA, who have studied myelination in the brains of adults ages 23 to 80, reported in September that the coating peaks around age 39 —the same age at which participants hit top speeds in standard tests of motor abilities.

100 trillion Minimum number of neural connections, or synapses, in the human brain. That is at least 1,000 times the number of stars in our galaxy. British researchers reported in December that genes involved in the workings of synapses account for about  7 percent of our genome.

50 Depth, in nanometers, of the smallest grooves detectable by a human fingertip (that is about 2 millionths of an inch). Most of the 2 billion or so nerve endings in the outermost layer of our skin sense pain; those dedicated to temperature allow us to detect differences as small as 0.01 degree Fahrenheit.

2,000 Number of slices created from the cerebral cortex of a mouse by Harvard University scientists . The researchers will image each slice under an electron microscope and then build a 3-D picture of all of the brain’s connections. Someday, similar maps of human brains may yield clues to mental illness, memory, and personality traits.

1 billion Number of neurons, linked by  10 trillion synapses, in a brain simulation developed by IBM and Lawrence Berkeley National Lab , running on the Dawn supercomputer. Researchers are testing hypotheses about how the brain works. The real human brain contains about 100 billion neurons, so scientists are getting close—in raw numbers, at least.

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Nerve Impulse

Introduction, continuous conduction , saltatory conduction , resting membrane potential, action potential , polarization , depolarization, repolarization , refractory period , electrical synapses , chemical synapses , cns and nerve impulse, myelin sheath, axon diameter, temperature, what is a nerve impulse, how is a nerve impulse produced, what is the refractory period, what are saltatory impulses.

Nerve impulse was discovered by British Scientist Lord Adrian in the 1930s. Owning to the importance of this discovery, he was awarded Noble Prize in 1932. Nerve Impulse is a major mode of signal transmission for the Nervous system. Neurons sense the changes in the environment and as a result, generate nerve impulses to prepare the body against those changes.

A nerve Impulse is defined as a wave of electrical chemical changes across the neuron that helps in the generation of the action potential in response to the stimulus. This transmission of a nerve impulse across the neuron membrane as a result of a change in membrane potential is known as Nerve impulse conduction.

It is a change in the resting state of the neuron. Due to nerve impulses, the resting potential is changed to an action potential to conduct signals to the target in response to a stimulus. The stimulus can be a chemical, electrical, or mechanical signal.

The action potential is a result of the movement of ions in and out of the cell. Particularly the ions included in this process are sodium and potassium ions. These ions are propagated inside and outside the cell through specific sodium and potassium pumps present in the neuron membrane. The transmission of a nerve impulse from one neuron to another neuron is achieved by a synaptic connection (synapse) between them. It is thus a mode of communication between different cells.

The speed of nerve impulse propagation varies in different types of cells. The rate of transmission and generation of nerve impulses depends upon the type of cell. Besides, Myelin Sheath also helps in accelerating the rate of signal conduction (about 20 times). Generally, the speed of nerve impulses is 0.1-100 m/s.

Mechanism of Nerve Impulse Conduction

Nerve impulse conduction is a major process occurring in the body responsible for organized functions of the body. So, for the conduction of nerve impulses, there are two mechanisms:

Continuous conduction
Saltatory conduction

Continuous nerve impulse conduction occurs in non-myelinated axons. The action potential travels along the entire length of the axon. Hence, more time is taken in generating and then transmit nerve impulses during an action potential.

Continuous conduction requires more energy to transmit impulses and is a slower process (approximately 0.1 m/s). It delays the process of conducting signals because it uses a higher number of ion channels to alter the resting state of the neuron.

Saltatory is faster than continuous conduction and occurs in myelinated neurons. In myelinated neurons, myelinated sheaths are present. Between these myelinated sheaths, unmyelinated gaps are presently known as the nodes of Ranvier. Nerve impulse propagates by jumping from one node of Ranvier to the next. This makes the process of nerve impulse faster as the nerve impulse does not travel the entire length of the axon ( this happens in the case of continuous conduction). The nerve impulse travels at a speed of 100 m/s in saltatory conduction.

The number of channels utilized in saltatory conduction is less than in continuous conduction due to which delay of nerve impulse does not occur. This mode of nerve impulse transmission utilizes less energy as well.

If you consider the axon as an electrical wire or loop, nerve impulse that travels along the axon as current, and the charged particles ( sodium and potassium ions) as the electron particles then the process can be understood quite easily. As the flow of current in a wire occurs at a specific voltage only, similarly the conduction of nerve impulse occurs when a stimulus has a maximum threshold value of -55 millivolts. This is essential for altering the resting membrane state to action membrane potential.

When the voltage has the required number of electron particles it conducts current. Similarly, in the case of nerve impulse conduction, the neurons of the stimulus must have a threshold value for causing the movement of ions across the length of the axon (for conducting nerve impulse) by opening the voltage-gated ion channels.

Process of transmission of Nerve Impulse

For the transmission of a nerve impulse, the stages are below:

Polarization
Repolarization
Refractory Period

Before going into the details of the process of nerve impulse transmission, let’s first discuss action and resting potential states.

The resting membrane potential refers to the non-excited state of the nerve cell at rest when no nerve impulse is being conducted. The resting membrane potential of the nerve cell is -70 mV. It is a static state and both the sodium and potassium channels are closed during this state maintaining a high concentration of sodium ions outside and high potassium ions concentration inside the cell.

An action potential occurs when the nerve cell is in an excited state while conducting nerve impulses. In this situation, sodium channels open and potassium channels are closed. This results in a huge influx of sodium ions inside the cells which trigger the nerve impulse conduction. The action potential is +40 mV.

Polarization is the situation in which the membrane is electrically charged but non-conductive. It means it doesn’t conduct nerve impulses in this state. During polarization, the membrane is in a resting potential state. The concentration of sodium ions is about 16 times more outside the axon than inside. In contrast, the concentration of potassium ions is 25 times more inside the axon than outside.

The polarization state is also known as the “Unstimulated or non-conductive state”. Due to the difference in the concentration of ions inside and outside the membrane, a potential gradient is established ranging between -20-200mV ( in the case of humans, the potential gradient in the polarized state is near -70mV). In the polarized state, the axon membrane is more permeable to potassium ions instead of sodium ions and as a result, it causes rapid diffusion of potassium ions.

In the resting state, the membrane potential becomes electro-negatively charged due to the movement of positively charged potassium ions outside the cell and the presence of electro-negative proteins in the intracellular space.

It refers to a graded potential state because a threshold stimulus of about -55mV causes a change in the membrane potential. The threshold stimulus must be strong enough to change the resting membrane potential into action membrane potential.

This results in the alternation in the electro-negativity of the membrane because the stimulus causes the influx of sodium ions (electropositive ions) by 10 times more than in the resting state. For this, sodium voltage-gated channels open. The action potential state is based on the “All or none” method and has two possibilities:

If the stimulus is not more than the threshold value, then there will be no action potential state across the length of the axon.

If the stimulus is more than the threshold value, then it will generate a nerve impulse that will travel across the entire length of the axon.

It is a condition during which the electrical balance is restored inside and outside the axon membrane. Due to the high concentration of sodium ions inside the axoplasm, the potassium channels will open. During the repolarization state, the efflux of potassium ions through the potassium channel occurs. As a result of the opening of potassium voltage-gated channels, sodium voltage-gated channels will be closed. Thus, no sodium ions will move inside the membrane. Therefore, repolarization helps in maintaining or restoring the original membrane potential state.

Until potassium channels close, the number of potassium ions that have moved across the membrane is enough to restore the initial polarized potential state. As a result of this, the membrane becomes hyperpolarized and has a potential difference of -90 mV.

The refractory phase is a brief period after the successful transmission of a nerve impulse. During this period, the membrane prepares itself for the conduction of the second stimulus after restoring the original resting state. It persists for only 2 milliseconds.

During this, the sodium ATPase pump allows the re-establishment of the original distribution of sodium and potassium ions. The sodium and potassium ATPase pump, driven by using ATP, helps to restore the resting membrane state for the conduction of a second nerve impulse in response to the other stimulus. It causes the movement of ions against the concentration gradient. For every two potassium ions that move inside the cell, three sodium ions are transported outside. This process requires ATP because the movement of ions is against the concentration gradient of both ions.

The process of transmission of a nerve impulse from one neuron to the other, after reaching the axon’s synaptic terminal, is known as synapse. This transmission of the nerve impulse by synapses involves the interaction between the axon ending of one neuron (Presynaptic neuron) to the dendrite of another neuron (Postsynaptic neuron). There is space between the pre-synaptic neuron and post-synaptic neuron which is known as synaptic cleft or synaptic gap.

After transmitting from one neuron to another, the nerve impulse generates a particular response after reaching the target site. If somehow the synaptic gap doesn’t allow the passage of nerve impulse, the transmission of nerve impulse will not occur and consequently required response too.

Types of synapses

There are two types of synapses:

Electrical synapses
Chemical synapses

In electrical synapses, two neurons are connected through channel proteins for transmitting a nerve impulse. The nerve impulse travels across the membrane of the axon in the form of an electrical signal. The signal is transmitted in the form of ions and therefore it is much faster than chemical synapses.

In electrical synapses, the synaptic gap is about 0.2nm which also favours faster nerve impulse conduction.

In chemical synapses, the conduction of nerve impulses occurs through chemical signals. These chemical signals are neurotransmitters. In this type of nerve impulse conduction, the synaptic gap is more than electrical synapses and is about 10-20 nm. Due to this, the transmission of nerve impulses is slower than electrical synapses.

Neurons help in transmitting signals in the form of nerve impulses from the Central nervous system to the peripheral body parts. Neurons are a complex network of fibres that transmit information from the axon ending of one neuron to the dendrite of another neuron. The signal finally reaches the target cell where it shows a response.

In conducting nerve impulses, the following play a major role:

Axon- Helps in the propagation of nerve impulses to the target cell.
Dendrites- Receive the signals from the axon ends.
Axon Ending- Acts as a transmitter of signals.

Axon plays a major role in the process by transmitting signals in the form of nerve impulses via synapses to the target cells. The neuron is responsible for transferring signals to three target cells:

Another neuron

And this results in the contraction of muscle, and secretion by glands and helps neurons to transmit action potential.

Factors Affecting the Speed of Nerve Impulse

The following are some major factors that affect the speed of nerve impulses:

Myelin sheath is present around the neuron and functions as an electrical insulator. Due to this sheath, an action potential is not formed on the surface of the neuron. This Myelin sheath has regular gaps, where it is not present, called nodes of Ranvier. An action potential can form at these gaps and impulse will jump from node to node by saltatory conduction. This can be a factor in increasing the speed of nerve impulses from about 30-1 m/ to 90-1 m/s.

As the axon diameter increase, the speed of nerve impulses increases as well. This is because a larger axon diminishes the ion leakage out of the axon. This helps in maintaining the membrane potential and thus favours faster nerve impulses.

Temperature cause changes in the rate of diffusion of ions across the neuron membrane. Temperature directly correlates with the transmission of nerve impulses. If the temperature is higher, the rate of diffusion of sodium and potassium ions will be high and the axon will become depolarized quickly which will cause a faster nerve impulse conduction.

A nerve impulse is thus an important signal transduction mode for triggering a response in major body parts due to a strong stimulus. Any distraction in this process can have drastic effects on the body.

Frequently Asked Questions

A nerve impulse is a wave of electrochemical changes that travel across the plasma membrane and helps in the generation of an action potential. Signals are propagated along the nerve fibres in the form of nerve impulses.

A nerve impulse is produced when a stimulus acts on the nerve fibre, resulting in electrochemical changes across the nerve membrane. These electrochemical changes cause depolarization of the membrane resulting in the generation of nerve impulses.

It is a short duration of time during which a new nerve impulse cannot be generated in a neuron, after initiation of a previous action potential. This period occurs at the end of action potential and limits the speed at which nerve impulses can be generated in a nerve fibre.

These are nerve impulses that jump from one node to another and are seen only in myelinated nerve fibres. Saltatory conduction increases the speed at which a nerve signal is conducted down the length of an axon.

Lodish, H; Berk, A; Kaiser, C; Krieger, M; Bretscher, A; Ploegh, H; Amon, A (2000). Molecular Cell Biology (7th ed.). New York, NY: W. H. Freeman and Company. p. 695.
Marieb, E. N., & Hoehn, K. (2014). Human anatomy & physiology. San Francisco, CA: Pearson Education Inc.

Why myelinated mammalian nerves are fast and allow high frequency

University of Alabama at Birmingham researchers, for the first time ever, have achieved patch-clamp studies of an elusive part of mammalian myelinated nerves called the Nodes of Ranvier. At the nodes, they found unexpected potassium channels that give the myelinated nerve the ability to propagate nerve impulses at very high frequencies and with high conduction speeds along the nerve. Both qualities are necessary for fast conduction of sensations and rapid muscle control in mammals -- keys to an animal's survival in a predator-prey world.

Discovered by French scientist Louis-Antoine Ranvier in 1878, these tiny nodes have been known since 1939 to act like relay stations placed about 1 millimeter apart along the myelinated nerve to conduct mammalian nerve impulses at rates of 50 to 200 meters per second. Between each bare node, the nerve is wrapped with insulating sheaths of myelin. When the nerve fires, the electrical impulse hops from one node to the next, moving 100-times faster than the nerve impulse of an unmyelinated nerve. Neuroscientists have long known that release and uptake of ions at the nerve cell membrane is the mechanism of electrical nerve impulses. But whether any potassium ion channels were present in the Nodes of Ranvier -- and if so, what type -- has been a matter of debate for decades because no one had been able to successfully apply patch clamps to the 1 to 2 micron-wide nodes of intact nerves in mammals.

In a study published in the Cell Press journal Neuron , Jianguo Gu, Ph.D., his postdoctoral fellow Hirosato Kanda, Ph.D., and other colleagues at UAB report that two ion channels called TREK-1 and TRAAK act as the principal potassium channels in the Nodes of Ranvier of a rat myelinated nerve. More importantly, they showed that those two channels at the Nodes of Ranvier were required for high-speed and high-frequency saltatory, or "hopping," conduction along myelinated afferent nerves. Knockdown of the channels reduced nerve conduction speed by 50 percent, and behavioral experiments showed that knockdown in the nerve reduced a rat's aversive reaction to a flick of its whisker.

In the classic experiments that led to a Nobel Prize in 1963 for the nerve impulse mechanism, nerves used a voltage-gated potassium channel (meaning a change in voltage makes it fire) to release potassium ions from an unmyelinated squid giant nerve. Gu and his colleagues initially expected to find such channels at the Nodes of Ranvier.

However, their earliest experiments confounded that expectation -- so much so that they dropped the study for a year. When they added known inhibitors of voltage-gated potassium channels, they saw no significant decrease in the electrical spikes at the Node of Ranvier. That finding challenged dogma, and it meant some other unidentified potassium channel or channels instead were serving as the workhorses at each node.

Possible candidates included three members of a family of 15 proteins known as "leak" potassium channels, which are constitutively open rather than voltage-gated and were known to have large conductance, says Gu, the Edward A. Ernst, M.D., Endowed Professor and director for pain research in the UAB Department of Anesthesiology and Perioperative Medicine's Division of Molecular and Translational Biomedicine. Gu's lab found that two of them, TREK-1 and TRAAK, are the active channels in the Nodes of Ranvier. Their tests to show this included the pressure-patch-clamp recording technique the researchers developed for the nodes, along with immunohistochemical, genetic and pharmacological approaches.

Furthermore, the UAB team found that TREK-1 and TRAAK -- which are thermosensitive and mechanosensitive two-pore-domain potassium channels -- are highly clustered at the nodes of the rat trigeminal A-beta nerve, with a current density that is 3,000-fold higher than that of the cell body.

Leak potassium channels and voltage-gated potassium channels act to repolarize the nerve membrane after a nerve impulse, known as an action potential. TREK-1 and TRAAK in the Nodes of Ranvier acted quite differently from the voltage-gated potassium channels that are found in the cell body, or soma, of the rat nerve. During a stimulation of the soma at 50-times per second, the action potentials that use the voltage-gated potassium channels typically failed. But Gu and colleagues found that action potentials at the Nodes of Ranvier with the "leak" channels showed no significant failures at stimulation frequencies up to 200-times per second.

In other words, the two leak potassium channels allowed very rapid repolarization at the Nodes of Ranvier, and high frequency as well as rapid conductance of the myelinated rat nerves. Interestingly, the TREK-1 and TRAAK two-pore-domain potassium channels appeared to form heterodimers in the Nodes of Ranvier.

Gu says these new fundamental findings have implications in neurological diseases or conditions where nodal dysfunctions affect action potential conduction. These include carpal tunnel syndrome, Guillain-Barré syndrome, multiple sclerosis, spinal cord injuries and amyotrophic lateral sclerosis.

Nervous System
Food Additives
Brain Injury
Neuroscience
Molecular Biology
Cell Biology
Sciatic nerve
Local anesthetic
Optic nerve
Oculomotor nerve
Spinal cord

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Materials provided by University of Alabama at Birmingham . Original written by Jeff Hansen. Note: Content may be edited for style and length.

Journal Reference :

Hirosato Kanda, Jennifer Ling, Sotatsu Tonomura, Koichi Noguchi, Sadis Matalon, Jianguo G. Gu. TREK-1 and TRAAK Are Principal K Channels at the Nodes of Ranvier for Rapid Action Potential Conduction on Mammalian Myelinated Afferent Nerves . Neuron , 2019; DOI: 10.1016/j.neuron.2019.08.042

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New Research Shows How Nerve Impulses Travel, May Offer Insights to Effects of MS Demyelination

by Ana Pena PhD | January 28, 2020

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Nerve impulses travel in a “dual cable” with myelin , playing additional roles to what was previously thought, new research has found. This discovery advances human knowledge of how brain connections work, and may help scientists understand more accurately what happens when myelin is lost — which is what occurs in diseases like multiple sclerosis (MS).

The study reporting the findings, titled “ Saltatory Conduction along Myelinated Axons Involves a Periaxonal Nanocircuit , ” was published in the journal Cell .

Nerve cell fibers, or axons , of vertebrates — animals with backbones, including humans — are covered by compact layers of a lipid -rich (fatty) substance known as myelin.

Myelin serves as a kind of electrical insulator that makes nerve impulses travel fast, so as to maintain high-speed communication between nerve cells, across the peripheral and central nervous systems (brain and spinal cord). In most densely myelinated axons, the conduction velocity can reach 70–120 meters per second , the speed of a race car.

At the basis of this rapid conduction are myelin-free gaps, called nodes of Ranvier , placed along the axon.

Nerve impulses, known as action potentials , can propagate quickly along the axon because they “jump” from one node of Ranvier to the next, a process known as saltatory conduction . An impulse jumps from node to node down the full length of an axon, speeding its arrival and transmission to the next nerve cell, compared with action potentials that travel along unmyelinated axons.

Scientists have known about this process for many decades. But they had been missing, until now, one piece of the detailed picture of how these electrical circuits take place, and what happens when myelin is damaged, such as in demyelinating diseases like MS.

While the view that myelin is an insulator with minimal or no electrical activity had been widely accepted, some scientists have proposed alternative models in which impulses can actually travel inside myelin or just below it.

Now, a team led by researchers at the Netherlands Institute for Neuroscience (NIN) sought to further assess signal transmission in myelinated neurons. They used a new technique that makes electrical currents visible, called high-speed optical recordings, and combined it with computational modeling to determine the specific properties of myelin sheaths in rat neurons.

The team also used a high-resolution microscopy technique, called electron microscopy , to measure the distance between the nerve cell membrane — the border that separates the nerve cell from the external environment — and the myelin sheath.

The evidence showed that the axon and the myelin sheath surrounding it are separated, creating a second conduction pathway that runs just below the myelin sheaths and above the nerve cell membrane, known as the submyelin space.

The distance between the nerve cell and myelin sheath turned out to be 12 nanometers, which corresponds to a size 10,000 times thinner than a human hair.

Such observations match a proposed model for the transmission of nerve impulses referred to as the “double cable.”

“All the findings together showed that instead of being an insulating sheath, myelin creates an additional layer like coaxial cables producing multiple waves of electrical potentials traveling in a more complicated manner than was envisioned earlier,” Maarten Kole, PhD, group leader at NIN and the study’s senior author, said in a press release .

According to the team, the findings open new avenues to understand how brains warrant the rapid spread of impulses, and how damage to the myelin sheath and submyelin spaces “may cause the conduction impairments observed in demyelinating diseases.”

The findings also allow researchers to fine-tune their models, and create tools to better understand such diseases.

In patients with MS, in particular, myelin loss leads to a decline in strength, balance, and coordination, limiting a person’s mobility. The team believes that, to better treat and prevent MS, it is important to know exactly how myelin works — and to predict what happens if it stops working.

“Our work now may provide reliable predictions of how impulses travel along the highways without myelin,” said Kole, also a professor at Utrech University , in the Netherlands.

“This finding contributes to the understanding of the cellular changes occurring in MS,” he said.

The research project was funded by the European Research Council (ERC), the National Multiple Sclerosis Society , and the Netherlands Organization for Scientific Research .

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How does a nerve impulse travel through the body?

The information acquired at the dendritic tip of a nerve cell sets off a chemical reaction that creates an electrical impulse. this impulse travels from the dendrite to the cell body and then along the axon to its end. at the end of the axon the electrical impulse sets off the release of some chemicals. these chemicals cross the gap or synapse and start a similar electrical impulse in a dendrite of the next neuron. a similar synapse finally allows the delivery of such impulse from neurons to other cells such as muscles or glands..

define nerve impulse which structure in a neuron help to conduct a nerve impulse :

i} towards the cell

ii} away from the cell body

What are the scheme of travelling of nerve impulse in the body?

COMMENTS

42.2: The Mechanism of Nerve Impulse Transmission
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FULL STORY. Scientists have proved a 60-year-old theory about how nerve signals are sent around the body at varying speeds as electrical impulses. Researchers tested how these signals are ...
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Like the heart, lungs, and stomach, the nervous system is made up of specialized cells. These include nerve cells (or neurons) and glial cells (or glia ). Neurons are the basic functional units of the nervous system, and they generate electrical signals called action potentials, which allow them to quickly transmit information over long distances.
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Nerve Impulse
Nerve impulse propagates by jumping from one node of Ranvier to the next. This makes the process of nerve impulse faster as the nerve impulse does not travel the entire length of the axon ( this happens in the case of continuous conduction). The nerve impulse travels at a speed of 100 m/s in saltatory conduction.
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Myelin sheath and myelin function are therefore the same, to increase the speed of nerve impulses. The amount of myelin in the body increases throughout development, from fetal development up until maturity, with the myelination in the prefrontal cortex being the last to complete in the 2nd or 3rd decade. The more myelin and myelination an ...
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Why myelinated mammalian nerves are fast and allow high frequency
In the classic experiments that led to a Nobel Prize in 1963 for the nerve impulse mechanism, nerves used a voltage-gated potassium channel (meaning a change in voltage makes it fire) to release ...
New Research Shows How Nerve Impulses Travel, May Offer Insight in
Nerve impulses, known as action potentials, can propagate quickly along the axon because they "jump" from one node of Ranvier to the next, a process known as saltatory conduction. An impulse ...
Nerve Impulse
Nerve impulses travel just as fast through the network of nerves inside the body. The axons of many neurons, like the one shown here, are covered with a fatty layer called myelin sheath. The sheath covers the axon, like the plastic covering on an electrical wire, and allows nerve impulses to travel faster along the axon. ...
Stimulating an axon causes impulses to travel both ways?
If you cut a piece of that axon, rotate it 180 degrees and join it back in the cutting points, it will conduct the action potential the same way. That being said, imagine that you stimulate that axon at a given point. There will be two action potentials, going to opposite ways: unmyelinated (A) and myelinated (B) nerve cells.
neuroscience
You've got a few things mixed up here: A signal may travel down a pathway, passing through several neurons (e.g. around 4-8). However, this signal is not always in the same form: From one end of a neuron to the other, it is merely an electric potential which travels down the neuron's cell membrane (from the dendrite to the axon hillock, where the cell decides whether to carry the signal on; if ...
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Q. Nerve impulse travel through synapse with the help of ____. Q. What is synapse how does the nerve impulse cross the synapse. Q. define nerve impulse which structure in a neuron help to conduct a nerve impulse : i} towards the cell. ii} away from the cell body. Q.

42.2: The Mechanism of Nerve Impulse Transmission

Nerve Impulse Transmission within a Neuron

Neuronal Charged Membranes

Resting Membrane Potential

Action Potential

Myelin and the Propagation of the Action Potential

Synaptic Transmission

Chemical Synapse

Electrical Synapse

Signal Summation

​​​​​Synaptic Plasticity

Long-term Potentiation (LTP)

Long-term Depression (LTD)

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11.41: Nerve Impulse

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Numbers: The Nervous System, From 268-MPH Signals to Trillions of Synapses

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Nerve Impulse

Mechanism of Nerve Impulse Conduction

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Why myelinated mammalian nerves are fast and allow high frequency

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New Research Shows How Nerve Impulses Travel, May Offer Insights to Effects of MS Demyelination

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