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Behaviour of neuron when membrane potential is maintained at threshold potential or more

Behaviour of neuron when membrane potential is maintained at threshold potential or more


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Via an external electrode the membrane potential of a neuron or group of neurons can be increased from resting potential of -70 mV to -50 mV or more. This will cause them to fire an action potential. What happens if the electrode maintains the membrane potential at -50 mV or more for say 1 minute? Initially it should fire once, but then it will not reach the resting potential, will it stop firing or keep on firing continuously since it is above threshold potential? Will this kill the neuron or make it malfunction permanently?


Before I start, I should point out that in order to change the membrane potential (known as the Vm) of a neuron you really need an internal electrode - so that you can pump current in to it, so increasing the potential above the resting membrane potential (RMP). The RMP is simply the Vm of a neuron at rest, without any external meddling by pesky scientists (or synaptic inputs).

When you depolarise a neuron - in other words, make it less negatively charged, it will fire an action potential once it crosses the spike threshold. This value is different for different neurons, but -50mV is usually not enough to trigger an action potential - normally it's more in the range between -30 and -40. But let's say it does, as it doesn't change the thrust of the question.

The major part of what happens during an action potential is that sodium channels open, allowing the spike to fire. Once closed, these channels have a 'refractory period' - essentially a time out, during which they are less likely to open again. So even though your neuron is still above spike threshold, it can't fire because the channels can't open. (For the aficionados, you can actually think of this as the spike threshold becoming temporarily more positive - going up to, say, -20mV).

So your neuron doesn't fire again for, say, 10ms, until the sodium channels reactivate. Then it does. So you get a train of regularly spaced action potentials at a certain frequency. The more you depolarise the neuron, the faster this frequency becomes until a point where the channels just become totally inactivated and the neuron stops firing. If you hold the cell at this voltage for more than a few seconds, in general it will die.


Edit 2: On second thoughts, maybe secondlevel isn't quite correct. Assuming a the membrane potential is held at -50 mV, using a patch pipette, in whole-cell voltage clamp, then the neuron generally won't fire action potentials. Not as we know them anyway as the cell membrane potential is "clamped". This controls the open probability of ion channels and allows ions to flow in and out of the cell, which can be measured as currents.

Unless the membrane potential is controlled by injection of current, in "current-clamp" mode. This could be controlled in patch-clamp, or done via an external electrode, which would provide local current, but wouldn't be so well controlled.

Secondlevel is pretty much spot on, here's an image of a neuron stepped to approx -60 mV from -78 mV.

The below cell's voltage is not being controlled directly; it is a recording in current-clamp mode, being depolarized by injecting positive current. Action potentials do not occur in a proper voltage-clamp.

Note that the action potentials aren't entirely predictable, there's a bit of variability in the frequency, but they're roughly every 20 ms. Also, this is just one example, from one cell type. Other neurons will behave differently.


Threshold Potential

Whether the threshold potential is reached depends on the amount of charge transferred across the membrane. Figure 19.6 shows that the total charge transfer across the membrane required to produce excitation is approximately constant (k = xy or Q = IT). It is an approximate rectangular hyperbola (xy = k) over the sharply-bending region of the curve. The strength–duration (S-D) curve can be derived from the equation for the exponential charge of the membrane capacitance.

FIGURE 19.6 . Strength–duration curve for AP initiation in excitable membranes. The intensity of rectangular stimulating pulses is plotted against their duration for stimuli that are just sufficient to elicit an AP. The rheobase current and chronaxie (σ) are indicated.

The S-D curve deals only with the stimulus parameters (i.e. strength and duration of the applied current pulses) necessary to bring the membrane to threshold. It shows that the greater the duration of the applied pulse, the smaller the current intensity required to just excite the fiber. The asymptote parallel to the x-axis is the rheobase, which is the lowest intensity of current capable of producing excitation, even when the current is applied for infinite time (practically, >10 ms for myelinated nerve fibers). The asymptote parallel to the y-axis is the minimal stimulation time, which is the shortest duration of stimulation capable of producing excitation, even when huge currents are applied.

The usefulness of the rheobase is limited when comparing the excitability of one nerve with another because only the relative current intensity is meaningful. Furthermore, it is difficult to measure the stimulation time of a current with the intensity of the rheobase because it is an asymptote. Thus, a graphic measurement is made of the time during which a stimulus of double the rheobasic strength must act in order to reach threshold. This time is the chronaxie. Chronaxie values tend to remain constant regardless of geometry of the stimulating electrodes. The shorter the chronaxie, the more excitable the fiber. The chronaxie value for normal myelinated nerve fibers is about 0.7 ms. Some nerve pathologies in humans can be detected early by changes in their chronaxies.

Measurement of chronaxie in the laboratory is also valuable because it provides an easy method for measuring the value of the membrane time constant τm (see Chapter 18 ). In brief, the relationship between chronaxie (σ) and time constant (τm) is:

Thus, τm is 1.44 times the value of σ. Therefore, σ is analogous to a half-time for a first-order reaction, whose rate constant is the reciprocal of the τm (k=1/τm).

The S-D curve indicates that current pulses of very short duration (e.g. <0.1 ms) are less effective for stimulation. Thus, sinusoidal alternating current (AC) at frequencies above 10 000 Hz is less capable of stimulation. Another way to view this is that, because the membrane impedance decreases greatly at high frequencies (since the cell membrane is a parallel RC network), the pd that can be produced across the membrane by current flow across it (IR or IX drops) is very small. Hence, AC of very high frequency has less tendency to electrocute and the energy of such currents can be dissipated as heat in body tissues and thus may be used in diathermy for therapeutic warming of injured tissues.


Behaviour of neuron when membrane potential is maintained at threshold potential or more - Biology

Synaptic plasticity is the strengthening or weakening of synapses over time in response to increases or decreases in their activity. Plastic change also results from the alteration of the number of receptors located on a synapse. Synaptic plasticity is the basis of learning and memory, enabling a flexible, functioning nervous system. Synaptic plasticity can be either short-term (synaptic enhancement or synaptic depression) or long-term. 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 involved in storing memories.

Long-term potentiation and depression: Calcium entry through postsynaptic NMDA receptors can initiate two different forms of synaptic plasticity: long-term potentiation (LTP) and long-term depression (LTD). LTP arises when a single synapse is repeatedly stimulated. This stimulation causes a calcium- and CaMKII-dependent cellular cascade, which results in the insertion of more AMPA receptors into the postsynaptic membrane. The next time glutamate is released from the presynaptic cell, it will bind to both NMDA and the newly-inserted AMPA receptors, thus depolarizing the membrane more efficiently. LTD occurs when few glutamate molecules bind to NMDA receptors at a synapse (due to a low firing rate of the presynaptic neuron). The calcium that does flow through NMDA receptors initiates a different calcineurin and protein phosphatase 1-dependent cascade, which results in the endocytosis of AMPA receptors. This makes the postsynaptic neuron less responsive to glutamate released from the presynaptic neuron.

Short-term Synaptic Enhancement and Depression

Short-term synaptic plasticity acts on a timescale of tens of milliseconds to a few minutes. Short-term synaptic enhancement results from more synaptic terminals releasing transmitters in response to presynaptic action potentials. Synapses will strengthen for a short time because of either an increase in size of the readily- releasable pool of packaged transmitter or an increase in the amount of packaged transmitter released in response to each action potential. Depletion of these readily-releasable vesicles causes synaptic fatigue. Short-term synaptic depression can also arise from post-synaptic processes and from feedback activation of presynaptic receptors.

Long-term Potentiation (LTP)

Long-term potentiation (LTP) is a persistent strengthening of a synaptic connection, which can last for minutes or hours. 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: NMDA (N-Methyl-D-aspartate) receptors. 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 and Ca 2+ ions pass into the postsynaptic cell. Next, Ca 2+ ions entering the cell initiate a signaling cascade that causes a different type of glutamate receptor, AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors, to be inserted into the postsynaptic membrane. Activated AMPA receptors allow positive ions to enter the cell.

Therefore, 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 so that the postsynaptic neuron is more likely to fire in response to presynaptic neurotransmitter release. Some drugs co-opt the LTP pathway 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. With the decrease in AMPA receptors in the membrane, the postsynaptic neuron is less responsive to the 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 trims unimportant connections, leaving only the salient connections strengthened by long-term potentiation.


Depolarization in different cells

The basic principle of depolarization is the same as described under the heading of physiology. However, different cells in the body respond to different stimuli and use different ion channels to undergo the process of depolarization. All this is in coherence with the function of that cell.

We will discuss the process of depolarization in
reference to neurons, endothelial cells, and cardiac cells.

Neurons

Neurons can undergo depolarization in response to a number of stimuli such as heat, chemical, light, electrical or physical stimulus. These stimuli generate a positive potential inside the neurons.

When the positive potential becomes greater than the threshold potential, it causes the opening of sodium channels. The sodium ions rush into the neuron and cause the shift in membrane potential from negative to positive.

Depolarization of a small portion of neuron generates
a strong nerve impulse. The nerve impulse travels along the entire length of
neuron up to the synaptic terminal.

Once the nerve impulse reaches the synaptic terminal, it causes release of neurotransmitters. These neurotransmitters diffuse across the synaptic cleft. They act as a chemical stimulus for the post-synaptic neuron. These neurotransmitters, in turn, cause the depolarization of postsynaptic neurons.

Endothelial cells

Vascular endothelial cells line the inner surface of blood vessels. These cells have structural capability to withstand the cardiovascular forces. They also play an important role in maintaining the functionality of the cardiovascular system.

These cells use the process of depolarization to alter their structural strength. When the endothelial cells are in a depolarized state, they have marked decreased structural strength and rigidity. In depolarized state, endothelial cells also cause a marked decrease in vascular tone of blood vessels.

Cardiac Cells

Depolarization of cardiac myocytes causes contraction of the cells and thus heart contraction occurs.

Depolarization first begins in the SA node, which is also called the cardiac pacemaker. SA node has automaticity. The resting membrane potential of SA node is less negative than that of other cardiac cells. This causes opening of sodium channels. Sodium ions continue to diffuse into the cells of SA node.

When the membrane potential becomes greater than the threshold potential, it causes the opening of Ca +2 channels. The calcium ions then rush in, causing depolarization.

Beginning in the SA node, the depolarization spreads
to atria and through AV node an AV bundle to Purkinje fibers causing
depolarization and contraction of ventricles.

Skeletal Muscles

The excitation of skeletal muscle by motor neurons causes the opening of voltage-gated sodium channels. The opening of sodium channels causes depolarization of the skeletal muscle.

The action potential from the motor neuron also travels through the T-tubules. It causes the release of Ca 2+ ions from the sarcoplasmic reticulum. Thus, contraction of skeletal muscle occurs. This entire process is also termed as excitation-contraction coupling.


Lesson Explainer: The Nerve Impulse Biology

In this explainer, we will learn how to explain how a resting potential is maintained and describe the electrical and chemical changes that occur during an action potential.

The human body contains over seven trillion nerves. Each signal these nerves send can travel at rapid speeds of up to 120 metres (almost 400 feet ) every second! This amazing evolutionary development allows us to think quickly and even act without thinking, to respond to our environment and aid our survival.

A neuron is a specialized cell found within the nervous system. Neurons’ function is to transmit information in the form of an electrical signal: a nerve impulse.

A nerve impulse is initiated by a stimulus, that is, a change in the internal or external environment. This stimulus triggers a receptor to send a nerve impulse to our central nervous system (CNS). The CNS, consisting of the brain and spinal cord, processes the information. Nerve impulses are then transmitted from the CNS to different organs that allow us to react to the stimulus appropriately. For example, a stimulus of touching a hot object will cause a series of nerve impulses to contract muscles in your arm to pull your hand away.

Definition: Neuron

A neuron is a specialized cell that transmits nerve impulses.

Let’s look at the structure of a neuron. Neurons come in many shapes and sizes however, most of them have a similar basic structure. Figure 1 shows an example of a neuron.

The nerve impulse first starts at the dendrites, then arrives at the cell body, which contains the nucleus of the neuron. The red arrows in Figure 1 show the path that the nerve impulse will take from the cell body and along the threadlike part of the neuron called an axon. Some neurons, like the one in Figure 1, have an insulating layer surrounding the axon called a myelin sheath. There are small gaps in the myelin sheath, called nodes of Ranvier, that play an important role in increasing the speed of a nerve impulse.

Key Term: Axon

An axon is the long threadlike part of a neuron along which nerve impulses are conducted.

To initiate and propagate a nerve impulse, a neuron must be excitable. What makes neurons electrically excitable?

The cytoplasm of neurons and the extracellular space are different fluids with different chemical compositions. As a consequence, they do not contain the same amounts of charged ions. There is normally an excess of positive charges in the extracellular space as we will see later in this explainer. This creates an electric tension, or potential, between both sides of the membrane, with the positive ions outside attracted by the negatively charged cytoplasm. In physics, this kind of electric force is called a voltage. The membrane is said to be polarized because of this difference of potential. Potentially, if there was a hole or a channel in the membrane, the positive ions would move freely inside until their concentration and charges equilibrate on both sides of the membrane.

The difference between the voltage inside the neuron’s cytoplasm and the extracellular space is called the membrane potential.

Key Term: Membrane Potential

The membrane potential, or potential difference, is the difference in electrical potential between the interior and exterior of a neuron.

When a neuron is not transmitting a nerve impulse, it is said to be at rest, and the membrane has its resting potential. The mechanism by which the resting potential is maintained is summarized in Figure 2.

Key Term: Resting Potential

The resting potential is the potential difference across the membrane of a neuron at rest (around

The resting potential is maintained through active transport by proteins embedded in the neuron membrane called sodium–potassium pumps. The sodium–potassium pump moves positively charged sodium (

) ions across the membrane using ATP energy. It requires energy, as sodium and potassium are being transported against their concentration gradients from an area of low concentration to an area of high concentration. For every three sodium ions pumped out of the neuron, two potassium ions are pumped in. This makes the voltage in the extracellular space more positive than the neuron’s cytoplasm. It also increases the concentration of potassium ions inside the neuron. In fact, the concentration of sodium ions is 10x–15x higher outside the neuron than inside, and the concentration of potassium is 30x higher inside the cell than outside!

The constant activity of sodium–potassium pumps plays a vital role in keeping neurons excitable. Ouabain, a plant-derived poison, has been used for several thousand years by West African tribes to make poisonous arrows. Ouabain is a potent blocker of the sodium–potassium pump as it attacks the nervous system, and one poisonous arrow is enough to rapidly kill any hunted animal, even an elephant.

Key Term: Sodium–Potassium Pump

The sodium–potassium pump maintains the resting potential of the axon membrane by transporting three sodium ions out and two potassium ions into the neuron.

The activity of the pump creates an imbalanced distribution of

across the membrane, with a higher concentration of

inside the neuron than outside and a higher concentration of

outside than inside. At rest, the membrane allows a minimal flow of these ions and remains 40x more permeable to

passively diffuses through pores called “leak” channels specific to these ions, moving down their concentration gradient from an area of high to low

concentration in the extracellular space.

The “leak” channels are always open, so the membrane is permeable to

remains forty times smaller. This net flow of ions ultimately lowers the membrane potential, as the outside of the cell becomes more positively charged.

Key Term: “Leak” Channels

“Leak” channels, or potassium ion channels, are always open making the neuron membrane permeable to potassium ions.

There are also negatively charged ions, such as chloride, and negatively charged proteins in a higher concentration inside the neuron. With the action of the sodium–potassium pump and “leak” channels, this contributes to making the extracellular space outside the neuron more positively charged than the cytoplasm inside the neuron. The membrane is polarized, achieving a resting potential of around

Example 1: Describing the Status of Ion Channels in Maintenance of the Resting Potential

When the resting potential is being maintained, are potassium ion channels (leak channels) open or closed?

Answer

When the neuron is at rest, the extracellular space is more positively charged than the neuron’s cytoplasm. The membrane is polarized, and the membrane potential is around

The resting potential is maintained primarily through active transport by proteins embedded in the neuron membrane called sodium–potassium pumps. The sodium–potassium pump moves positively charged sodium (

) ions across the membrane using ATP. It requires energy, as

are being transported against their concentration gradients from an area of low concentration to an area of high concentration. For every

ions that are pumped out of the neuron,

ions are pumped in. This makes the voltage in the extracellular space more positive than the neuron cytoplasm. It also increases the concentration of

concentration inside the neuron,

will also “leak” across the neuron membrane out of the cytoplasm into the extracellular space. It passively diffuses through pores called “leak” channels specific to

, moving down its concentration gradient from an area of high to low

concentration. “Leak” channels are always open, so the membrane is permeable to

. This lowers the membrane potential, as the outside of the cell is becoming more positively charged, achieving the resting potential of

Therefore, when resting potential is maintained, the potassium ion channels (leak channels) are open.

When the neuron is not at rest, it is conducting a nerve impulse called an action potential.

Action potentials are electrical signals that transmit information by the movement of charged ions across the membrane of a neuron as the action potential passes along it. This temporarily changes the potential difference at the particular point on the neuron where ions are moving.

The main stages of an action potential are

  1. depolarization,
  2. repolarization,
  3. Hyperpolarization,
  4. a brief refractory period during which another action potential cannot be generated.

The movement of ions in depolarization and repolarization is summarized in Figure 3.

Key Term: Action Potential

An action potential is the transient change in the potential difference across the neuron membrane when stimulated (approximately

Let’s look at depolarization first.

Depolarization is when the membrane potential at one point on the neuron reverses from negative to positive. This is initially caused by the activation of chemical receptors at synapses located at the dendrites of a neuron. The activation of these receptors triggers the opening of voltage-gated

channels that were previously shut, making the membrane more permeable to

diffuses into the neuron cytoplasm as it is less concentrated there than in the extracellular space due to the action of the sodium–potassium pump. The increased concentration of

makes the neuron cytoplasm less negatively charged as you can see in Figure 4. The increased positivity of the membrane potential causes more voltage-gated

channels to open. This means that

diffuses into the neuron at a faster rate, which continues until the membrane potential reaches a value of around

Key Term: Depolarization

Depolarization is a change in the membrane potential at one point in a neuron from negative to positive.

Key Term: Voltage-Gated Ion Channels

Voltage-gated ion channels are those that open and close in response to changes in the membrane potential of the cell and, as a result, enable a flow of ions across a membrane.

When the membrane potential has reached

channels close, and voltage-gated

can no longer enter the neuron.

is more concentrated in the neuron cytoplasm than in the extracellular space due to the action of the sodium–potassium pump, so

can now diffuse out. This lowers the membrane potential, and the neuron cytoplasm again becomes less positively charged than the extracellular space. This is called repolarization, as you can see in Figure 5.

Key Term: Repolarization

Repolarization is a change in the membrane potential at one point in a neuron from positive back to negative.

diffuses out of the neuron when the voltage-gated

channels open that the membrane potential temporarily becomes even more negative than its resting potential. This is called hyperpolarization.

Hyperpolarization causes the voltage-gated

channels to close, and the sodium–potassium pump resets the membrane to its resting potential. You can see this occurring in the final stage of Figure 3. This period of time is called the refractory period, during which no more action potentials can be generated as the voltage-gated

channels remain closed. Refractory periods last a very short time, usually between 0.001 and 0.003 seconds !

Key Term: Hyperpolarization

Hyperpolarization is a change in the membrane potential at one point in a neuron to more negative than its original resting potential.

Key Term: Refractory Period

The refractory period is a brief period immediately following an action potential during which a neuron is unresponsive to further stimulation and therefore cannot generate another action potential.

Example 2: Stating the Sequence of Stages in an Action Potential

The diagram provided shows the stages of an action potential, with each stage assigned a number. State the correct sequence of numbers.

Answer

An action potential is a change in the electrical potential of the neuron membrane as the nerve impulse passes along the neuron. Its main stages are depolarization, repolarization, hyperpolarization, and a brief refractory period.

Depolarization is when the electrical charge at one point on the neuron membrane reverses from negative to positive. This is caused by energy from a stimulus triggering the opening of voltage-gated

diffuses into the neuron cytoplasm. The increased concentration of

makes the neuron cytoplasm less negatively charged, which causes more voltage-gated

diffuses into the neuron at a faster rate until the membrane potential reaches around

can no longer enter the neuron. Voltage-gated

can diffuse out of the neuron cytoplasm. This lowers the membrane potential, and the neuron cytoplasm again becomes less positively charged than the extracellular space. This is called repolarization.

diffuses out of the neuron that the membrane potential becomes even more negative than its resting potential. This is called hyperpolarization, and it causes the voltage-gated

channels to close. The sodium–potassium pump resets the membrane to its resting potential in a period of time called the refractory period. During the refractory period, no more action potentials can be generated as the voltage-gated

Therefore, the correct sequence of events in an action potential is 4, 2, 6, 1, 5, 3.

Let’s look at the graph in Figure 6 showing how the membrane potential changes during an action potential.

  1. In stage 1, the resting potential is being maintained at stage 1, with the sodium–potassium pump and “leak” channels keeping the membrane potential at around

channels to open at stage 2, depolarizing the membrane to

channels open. Stage 3 shows repolarization of the membrane, as

Example 3: Describing the Events of an Action Potential

The graph provided shows how the potential difference across an axon membrane changes during the course of an action potential. What is happening during stage 2?

Answer

The resting potential is being maintained at stage 1, with the sodium–potassium pump keeping the membrane potential at around

mV . A stimulus has caused voltage-gated

channels to open at stage 2, depolarizing the membrane to

channels open. Stage 3 shows repolarization of the membrane, as

diffuses out of the axon. Stage 4 shows hyperpolarization of the membrane, overshooting the resting potential. Following this refractory period, the resting potential is reset in stage 5, returning the membrane potential to

Therefore, at stage 2, a stimulus has triggered the opening of voltage-gated sodium ion channels, and sodium ions depolarize the membrane.

Example 4: Describing the Events of an Action Potential

The graph provided shows how the potential difference across an axon membrane changes during the course of an action potential. What is happening during stage 3?

Answer

The resting potential is being maintained at stage 1, with the sodium–potassium pump keeping the membrane potential at around

mV . A stimulus has caused voltage-gated

channels to open at stage 2, depolarizing the membrane to

channels open. Stage 3 shows repolarization of the membrane, as

diffuses out of the axon. Stage 4 shows hyperpolarization of the membrane, overshooting the resting potential. Following this refractory period, the resting potential is reset in stage 5, returning the membrane potential to

Therefore, at stage 3, voltage-gated potassium ion channels open, and potassium ions diffuse out of the axon.

An action potential is then propagated from one end of the neuron’s axon to the other, in one direction only. This propagation is referred to as a wave of depolarization.

This is because as one section of the axon’s membrane depolarizes, positively charged

moves into the axon cytoplasm, as you can see in the green section of stage 1 in Figure 7.

Voltage-gated sodium channels next to the initial site of depolarization get activated so that sodium diffuses along the axon to depolarize the next section as you can see in stage 2 in Figure 8. This triggers voltage-gated

channels in this next section to open, and the membrane at this point becomes fully depolarized.

The wave of depolarization can only travel in one direction, as the section behind the depolarized section in stage 3 is repolarizing, as you can see in Figure 9. The voltage-gated

diffuses out of the axon, making it more negative than the extracellular space, and the membrane hyperpolarizes. During this refractory period, the voltage-gated

channels remain shut, so no

can move into the axon and the

in the wave of depolarization cannot diffuse backward.

The strength of a stimulus determines whether an action potential will be generated. If the stimulus passes a threshold value, it will always trigger an action potential. If the stimulus does not pass this value, no action potential will be generated. Therefore, action potentials are called all-or-nothing responses.

Though the action potential will always be the same size, if a stimulus is stronger, the frequency of action potentials will be higher and so more will be generated per unit time.

Key Term: The All-or-Nothing Principle

The all-or-nothing principle states that if a stimulus is large enough to pass a threshold value, an action potential of the same size will always be generated. If the stimulus is not large enough to pass this value, no action potential will be generated.

Three factors affect the speed of transmission of an action potential.

At higher temperatures, ions diffuse faster as they have more kinetic energy. This increases the speed of the action potential. At temperatures above

, however, proteins such as the sodium–potassium pump start to denature, which causes transmission rate to drop.

The diameter of the axon also affects the speed of an action potential. The larger the diameter, the faster the transmission, as the diffusing ions encounter less resistance. This is like if lots of people were trying to walk along a wide corridor, it would be much easier than the same number of people walking along a narrow one!

Whether or not an axon is myelinated also affects the speed of transmission. Myelinated axons conduct nerve impulses faster than nonmyelinated axons. The speed of propagation of a nonmyelinated axon is around 12 metres per second , whereas propagation along a myelinated axon can reach up to 140 metres per second !

The voltage-gated ion channels are only found in the nodes of Ranvier in myelinated axons, so depolarization can only occur at these points. This means that the action potential “jumps” from one node to the next as represented by the pink arrows in Figure 10. This process is called saltatory conduction, from the Latin word meaning “leap,” and it speeds up the transmission as less time is taken in opening and closing ion channels.

Comparatively, lots of ion channels are opening and closing in the nonmyelinated axon in Figure 10, so the speed of propagation of the action potential is much slower.

Key Term: Saltatory Conduction

Saltatory conduction describes how action potentials propagate along a myelinated axon by “jumping” from one node of Ranvier to the next, increasing the speed of conduction compared to nonmyelinated axons.


How Is Resting Membrane Potential Maintained?

The resting membrane potential of a cell is maintained by the sodium-potassium pump and is possible because the membrane itself is not very permeable to ions. The sodium-potassium pump uses the energy stored in ATP to pump sodium and potassium across the membrane.

The resting membrane is established and maintained because the phospholipid bilayer contains a middle section that repels charged molecules and ions. As a result, the ions can only pass through the membrane if there are channels for the ions. Certain molecules, such as DNA and many negatively charged protons, contribute a negative charge to the cell and cannot diffuse out along their concentration gradient.

These negatively charged molecules in the cell allow the cell to maintain a concentration gradient by pumping the positively charged cations alone. Although both sodium and potassium ions are positively charged, the negative-inside membrane potential is maintained because the sodium-potassium pump doesn't pump the same number of each ion. Instead, for every cycle of the sodium-potassium pump, one ATP molecule is used to pump two potassium ions in and three sodium ions out. More positive ions leaving the cell means that the membrane interior is getting more and more negative overall.

Using these pumps and controlling other cation channels in the membrane, the cell is able to maintain a negative resting 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 16.13 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.

Figure 16.13. Nodes of Ranvier are gaps in myelin coverage along axons. Nodes contain voltage-gated K+ and Na+ channels. Action potentials travel down the axon by jumping from one node to the next.


6.5.12 Distinguish between type I and type II diabetes.

Type I diabetes

Type II diabetes

The onset is usually early, sometime during childhood.

The onset is usually late, sometime after childhood.

&beta cells do not produce enough insulin.

Target cells become insensitive to insulin.

Diet by itself cannot be used to control the condition. Insulin injections are needed to control glucose levels.

Insulin injections are not usually needed. Low carbohydrate diet can control the condition.


UNIT 9 NERVOUS COORDINATION

Neurones are cells adapted for the rapid transmission of electrical impulses to do this, they have long thin processes called axons. Sensory neurones transmit impulses from receptors to the central nervous system (brain and spinal cord). Motor neurones transmit impulses from the central nervous system to effectors. Relay neurones transmit impulses within the central nervous system. Sensory, relay and motor neurones are found in series in reflex arcs that control fast, automatic responses to stimuli.
Neurones have a resting potential, which is a potential difference across their membranes, with the inside having a negative potential compared with the outside this potential difference is about −70 mV. An action potential is a rapid reversal of this potential, caused by changes in permeability of the cell surface membrane to potassium and sodium ions. Action potentials are always the same size. Information about the strength of a stimulus is given by the frequency of action potentials produced. Action potentials are propagated along axons by local circuits that depolarise regions of membrane ahead of the action potential. This depolarisation stimulates sodium ion voltage-gated channels to open, so that the permeability to sodium increases and the action potential occurs further down the axon.
Action potentials may be initiated within the brain or at a receptor. Environmental changes result in permeability changes in the membranes of receptor cells, which in turn produce changes in potential difference across the membrane. If the potential difference is sufficiently great and above the threshold for the receptor cell, this will trigger an action potential in a sensory neurone.

Functions of the Nervous System • Detect changes and feel sensations.
• Initiate responses to changes.
• Organize and store information.
Nervous System Divisions
• Central nervous system (CNS): brain and spinal cord.
• Peripheral nervous system (PNS): 12 pairs of cranial nerves and 31 pairs of spinal nerves.
Nerve Tissue: neurons (nerve fibers) and specialized cells (Schwann, neuroglia)
• Neuron cell body contains the nucleus cell bodies are in the CNS or in the trunk and are protected by bone.
• Axon carries impulses away from the cell body dendrites carry impulses toward the cell body.
• Schwann cells in PNS: Layers of cell membrane form the myelin sheath to electrically insulate neurons nodes of Ranvier are spaces between adjacent Schwann cells. Nuclei and cytoplasm of Schwann cells form the neurolemma, which is essential for regeneration of damaged axons or dendrites.
• Oligodendrocytes in CNS form the myelin sheaths microglia phagocytize pathogens and damaged cells astrocytes contribute to the blood–brain barrier.
• Synapse: the space between the axon of one neuron and the dendrites or cell body of the next neuron. A neurotransmitter carries the impulse across a synapse and is then destroyed by a chemical inactivator. Synapses make impulse transmission one way in the living person.
Types of Neurons
• Sensory: carry impulses from receptors to the CNS may be somatic (from skin, skeletal muscles, and joints) or visceral (from internal organs).
• Motor: carry impulses from the CNS to effectors may be somatic (to skeletal muscle) or visceral (to smooth muscle, cardiac muscle, or glands). Visceral motor neurons make up the autonomic nervous system.
• Interneurons: entirely within the CNS.

The Nerve Impulse • Polarization: neuron membrane has a (+) charge outside and a (+) charge inside.
• Depolarization: entry of Na ions and reversal of charges on either side of the membrane.
• Impulse transmission is rapid, often several meters per second.
• Saltatory conduction: in a myelinated neuron only the nodes of Ranvier depolarize increases speed of impulses.
The Spinal Cord
• Functions: transmits impulses to and from the brain, and integrates the spinal cord reflexes.
• Location: within the vertebral canal extends from the foramen magnum to the disc between the 1stand 2nd lumbar vertebrae.
• Cross-section: internal H-shaped gray matter contains cell bodies of motor neurons and interneurons external white matter is the myelinated axons and dendrites of interneurons.
• Ascending tracts carry sensory impulses to the brain descending tracts carry motor impulses away from the brain.
• Central canal contains cerebrospinal fluid and is continuous with the ventricles of the brain.
Spinal Cord Reflexes: do not depend directly on the brain
• A reflex is an involuntary response to a stimulus.
• Reflex arc: the pathway of nerve impulses during are flex: (1) receptors, (2) sensory neurons, (3) CNS with one or more synapses, (4) motor neurons, (5) effector that responds.
Meninges and Cerebrospinal Fluid (CSF)
• Three meningeal layers made of connective tissue: outer dura mater middle arachnoid membrane inner pia mater all three enclose the brain and spinal cord.
• Subarachnoid space contains CSF, the tissue fluid of the CNS.
The Autonomic Nervous System (ANS)
• Has two divisions: sympathetic and parasympathetic their functioning is integrated by the hypothalamus.
• Sympathetic division: dominates during stress situations responses prepare the body to meet physical demands.
• Parasympathetic division: dominates in relaxed situations to permit normal functioning.

Biology 8th edition, CAMPBELL AND REECE, SAN FRANCISCO, USA

The figure below shows the event that takes place in a chemical synapse:
a) What are the elements represented by the letters A to E?
b) What is the role of Ca2+ in the process?
c) What is the difference between an electrical synapse and a chemical synapse?

The figure below shows the change in membrane potential during the passage of a nerve impulse.
a) What is the resting potential of this neuron?
b) How is the resting potential maintained in the neuron?
c) Explain how ion movements bring about the change in membrane potential between points A and B on the graph?
d) How is the resting potential restored?
e) What is the refractory period?
f) How does the length of the refractory period limit the number of impulses which can pass along the axon?
g) Account for the blip at point X on the graph?

Suggest why:
a) Impulses travel in only one direction ay synapses.
b) If action potentials arrive repeatedly at a synapse, the synapse eventually becomes unable to transmit the impulse to the next neuron.

The table below shows the speed by which different axons conduct action potentials
a) Using data from the table, describe the effect of axon diameter on the speed of conductance of an action potential.
b) The data show that a myelinated axon conducts an action potential faster than an unmyelinated one. Explain why this is so.
c) What is the name of the cells whose membranes make the myelin sheath around some types of neurons?
d) State whether the presence of myelin or the diameter of the axon has the greater influence on the speed of conductance of an action potential. Use the information from the table to explain your answer.
e) The squid is an ectothermic animal. This means that its body temperature fluctuates with the temperature of the waters in which it lives. Suggest how this might affect the speed a squid conducts action potentials along its axon.


Objective

A neuron is frequently compared to electronic circuit as most of its properties can be modeled as electronic circuits. The membrane potential across the neuronal membrane is similar to the voltage of an electrical circuit. In neurons, this is known as potential difference which is due to the effects of charges across the membrane. Separation of charge is termed as voltage. In electrical circuits, voltage is acquired using a power source. The electrical circuit expresses current as it (current) is the movement of charges from one point to other point. In the neurons this affect is caused by movement of charged ions across cell membrane.

In this experiment, we modeled neuron as RC networks. Neuronal membrane has capacitive and resistive properties. Thus it often referred to as membrane resistance or membrane conductance. Membrane resistance is too high when most of the ion channels are closed. At this time few ions crosses the membrane. On the other hand, during depolarization events, in which many ion channels are open and the cell experiences large influxes and effluxes of ions, membrane conductance is said to be high. A capacitor consists of two conducting regions separated by an insulator. It works by accumulating a charge on one of the conducting surfaces. Electric fields are created as this charge builds. This field pushes charges on the other side of the insulator away. Similarly in the neuron the membrane is the insulator between the two conducting intra and extracellular fluids. Capacitance plays the most important role in action potential generation and propagation.

Figure.1.a. Schematic cartoon of neuron along with (The cartoon mechanism of a biological neuron showing stimulating electrode in the response electrode. Response electrode records the output behavior and stimulating electrodes provides the input)

Figure.1. b. RC properties

Bursting is an extremely diverse general phenomenon of the activation patterns of neurons in the central nervous system and spinal cord where periods of rapid spiking are followed by quiescent, silent, periods. Bursting Hardware neuron model with the simple excitable hardware neuron model.

We adopted the above mentioned RC circuit to generate burst phenomenon. We applied pulses at regular intervals to the RC circuit to create the burst .The pulses with time intervals will charge and discharge capacitors at regular intervals which may leads to the series of action potentials at regular intervals Since the models with adaptation, reproduce both spiking and bursting.



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