What is the significance of the undershoot that happens during the hyper polarization event?Does it serve a specific purpose?

Yes, it prevents the action potential from going backwards.

What happens if the sodium/potassium pump is nonfunctional and the membrane potential can't return to the resting membrane potential? Can another action potential be produced, or will the membrane potential never be able to reach the threshold again?

Hi, I'm a neurobio professor, and this is one of the biggest misconceptions in neuroscience. The pump plays no *direct* role in returning to resting potential. The pump simply maintains the concentrations gradients over a long time period. But: When an action potential occurs, only a tiny, tiny amount of ions (<0.001%) need to move across the membrane to change the membrane potential. This is because membrane potential changes are not determined by concentration changes, but by *permeability* changes. The membrane potential is a function of the relative permeability (through ion channels) of the membrane to each ion, and the equilibrium potential (E_ion) for that ion. The E_ion is determined by the concentration gradient set up by the pump. The membrane is hyperpolarized at the end of the AP because voltage-gated potassium channels have increased the permeability to K+. As they close, the membrane returns to the resting potential, which is set by permeability through the "leak" channels. Those are mostly K+ channels, so the membrane potential is still very close to E_K.

Why does people with one sort of epilepsy suffer from seizures while others don't? Is it because some sort of abnormality in the membrane potential?

Contrary to these other two answers, I think you're spot on with the mechanistic explanation. Of course, it gets much more complicated if you look into it. Fundamentally, the problem in epilepsy is that some resting membrane potentials in any of the clusters of cells in the brain can move closer to threshold. So, instead of needing to integrate enough excitatory signals to go from -70mv -> -55mV, someone with epilepsy might have a nucleus in the brain (a cluster of cell bodies) that only needs to depolarize from -60mV -> -55mV in order to fire action potentials. Genetic factors can cause this, but certain drugs can cause it as well, such as lamotrigine. Once this cluster of neurons recieves strong enough stimulus for the activation to spread (the stronger the stimulus, often the more neurons become involved), the entire cluster of neurons can easily depolarize at once, creating the characteristic waves of excitation seen in epilepsy. For example, in photosensitive epilepsy, intense visual stimuli cause a critical mass of neurons in the visual cortex to fire synchronously, initiating a wave of excitation.

How do synapses affect the speed with which a nerve impulse is transmitted?

Electrical synapses are present, but rare- where the synaptic cleft is negligible in length (i.e. impulses can pass directly from the terminal to a dendrite.) They are much more common in invertebrates.

are sodium and potassium gates ever open a the same time during the action potential?

As I am informed so far, there is no such moment during the generation of an action potential. As soon as potassium channels open, before that sodium channels close (repolarization).

are there any other types of neurons? If so then how many

Many different types, broadly categorized with respect to their shape or their function. Motor neurons, interneurons (AKA relay neurons) and sensory neurons are the traditional classifications with respect to function. Motor neurons transmit a signal to an 'effector' of some kind (a muscle or a gland perhaps), interneurons transmit signals between surrounding neurons, and sensory neurons 'receive' stimuli (interpreting the stimulus and integrating it).

Main content

Course: Biology library > Unit 33

Lesson 2: The neuron and nervous system

Q & A: Neuron depolarization, hyperpolarization, and action potentials

Q: Why does people with one sort of epilepsy suffer from seizures while others don't? Is it because some sort of abnormality in the membrane potential?

Contrary to these other two answers, I think you're spot on with the mechanistic explanation. Of course, it gets much more complicated if you look into it. Fundamentally, the problem in epilepsy is that some resting membrane potentials in any of the clusters of cells in the brain can move closer to threshold. So, instead of needing to integrate enough excitatory signals to go from -70mv -> -55mV, someone with epilepsy might have a nucleus in the brain (a cluster of cell bodies) that only needs to depolarize from -60mV -> -55mV in order to fire action potentials. Genetic factors can cause this, but certain drugs can cause it as well, such as lamotrigine. Once this cluster of neurons recieves strong enough stimulus for the activation to spread (the stronger the stimulus, often the more neurons become involved), the entire cluster of neurons can easily depolarize at once, creating the characteristic waves of excitation seen in epilepsy. For example, in photosensitive epilepsy, intense visual stimuli cause a critical mass of neurons in the visual cortex to fire synchronously, initiating a wave of excitation.

Google Classroom

Answer to #AskKhanAcademy Fall Finals 2015 question.

Question:

What causes the hyperpolarization and depolarization of membrane potential, and how does change in membrane potential trigger graded and action potentials for the transmission of signals?

– Vincent Tse

Answer:

Hi Vincent,

That’s a great question! Here is a written explanation, with links to some videos that may also help you.

Hyperpolarization and depolarization

At rest, a typical neuron has a resting potential (potential across the membrane) of

- 60

- 70

millivolts. This means that the interior of the cell is negatively charged relative to the outside.

See videos: Neuron resting potential description, Neuron resting potential mechanism

Hyperpolarization is when the membrane potential becomes more negative at a particular spot on the neuron’s membrane, while depolarization is when the membrane potential becomes less negative (more positive). Depolarization and hyperpolarization occur when ion channels in the membrane open or close, altering the ability of particular types of ions to enter or exit the cell. For example:

The opening of channels that let positive ions flow out of the cell (or negative ions flow in) can cause hyperpolarization. Examples: Opening of channels that let $K^{+}$ ‍ out of the cell or ${Cl}^{-}$ ‍ into the cell.
The opening of channels that let positive ions flow into the cell can cause depolarization. Example: Opening of channels that let ${Na}^{+}$ ‍ into the cell.

The opening and closing of these channels may depend on the binding of signaling molecules such as neurotransmitters (ligand-gated ion channels), or on the voltage across the membrane (voltage-gated ion channels).

Graded potentials

A hyperpolarization or depolarization event may simply produce a graded potential, a smallish change in the membrane potential that is proportional to the size of the stimulus. As its name suggests, a graded potential doesn’t come in just one size – instead, it comes in a wide range of slightly different sizes, or gradations. Thus, if just one or two channels open (due to a small stimulus, such as binding of a few molecules of neurotransmitter), the graded potential may be small, while if more channels open (due to a larger stimulus), it may be larger. Graded potentials don’t travel long distances along the neuron’s membrane, but rather, travel just a short distance and diminish as they spread, eventually disappearing.

See videos: Electrotonic and action potentials, Neuron graded potential description, Neuron graded potential mechanism

Action potential

Alternatively, a large enough depolarization event, perhaps resulting from multiple depolarizing inputs that happen at the same time, can lead to the production of an action potential. An action potential, unlike a graded potential, is an all-or-none event: it may or may not occur, but when it does occur, it will always be of the same size (is not proportional to the size of the stimulus).

An action potential begins when a depolarization increases the membrane voltage so that it crosses a threshold value (usually around $- 55$ ‍ $mV$ ‍).
At this threshold, voltage-gated ${Na}^{+}$ ‍ channels in the membrane open, allowing many sodium ions to rush into the cell. This influx of sodium ions makes the membrane potential increase very rapidly, going all the way up to about $+ 40$ ‍ $mV$ ‍.
After a short time, the sodium channels self-inactivate (close and become unresponsive to voltage), stopping the influx of sodium. A set of voltage-gated potassium channels open, allowing potassium to rush out of the cell down its electrochemical gradient. These events rapidly decrease the membrane potential, bringing it back towards its normal resting state.
The voltage-gated potassium channels stay open a little longer than needed to bring the membrane back to its resting potential. This results in a phenomenon called “undershoot,” in which the membrane potential briefly dips lower (more negative) than its resting potential.
Eventually, the voltage-gated potassium channels close and the membrane potential stabilizes at resting potential. The sodium channels return to their normal state (remaining closed, but once more becoming responsive to voltage). The action potential cycle may then begin again.

See videos: Electrotonic and action potentials, Neuron action potential description, Neuron action potential mechanism

Transmission of a signal by action potentials

The cycle above is described for just one patch of membrane. However, an action potential can travel down the length of a neuron, from the axon hillock (the base of the axon, where it joins the cell body) to the tip of the axon, where it forms a synapse with the receiving neuron.

See video: Anatomy of a neuron

This directional transmission of the signal occurs for two reasons:

First, when one patch of membrane (say, right at the axon hillock) undergoes an action potential, lots of ${Na}^{+}$ ‍ ions rush into the cell through that patch. These ions spread out laterally inside the cell and can depolarize a neighboring patch of membrane, triggering the opening of voltage-gated sodium channels and causing the neighboring patch to undergo its own action potential.
Second, the action potential can only travel in one direction – from the cell body towards the axon terminal – because a patch of membrane that has just undergone one action potential is in a “refractory period” and cannot undergo another.
The refractory period is primarily due to the inactivation of voltage-gated sodium channels, which occurs at the peak of the action potential and persists through most of the undershoot period. These inactivated sodium channels cannot open, even if the membrane potential goes above threshold. The slow closure of the voltage-gated potassium channels, which results in undershoot, also contributes to the refractory period by making it harder to depolarize the membrane (even once the voltage-gated sodium channels have returned to their active state).
The refractory period ensures that an action potential will only travel forward down the axon, not backwards through the portion of the axon that just underwent an action potential.

When the action potential reaches the end of the axon (the axon terminal), it causes neurotransmitter-containing vesicles to fuse with the membrane, releasing neurotransmitter molecules into the synaptic cleft (space between neurons). When the neurotransmitter molecules bind to ligand-gated ion channels on the receiving cell, they may cause depolarization of that cell, causing it to undergo its own action potential. (Some neurotransmitters also cause hyperpolarization, and a single cell may receive both types of inputs.)

See video: Neuronal synapses (chemical)

I hope that helps! Good luck with your finals studying!

Best wishes,

Emily (Khan Academy Biology)

References:

Animation: Voltage-gated channels and the action potential. (2015). In Essentials of anatomy & physiology: Online learning center. Retrieved from http://highered.mheducation.com/sites/0072943696/student_view0/chapter8/animation__voltage-gated_channels_and_the_action_potential__quiz_2_.html.

OpenStax College, Biology. (2015). How neurons communicate. In OpenStax CNX. Retrieved from http://cnx.org/contents/185cbf87-c72e-48f5-b51e-f14f21b5eabd@9.87:182/How-Neurons-Communicate.

Refractory period. (2015, July 8). Retrieved December 9, 2015 from Wikipedia: https://en.wikipedia.org/wiki/Refractory_period_%28physiology%29.

Reece, J. B., Urry, L. A., Cain, M. L., Wasserman, S. A., Minorsky, P. V., and Jackson, R. B. (2011). Neurons, synapses, and signaling. In Campbell biology (10th ed., pp. 1061-1078). San Francisco, CA: Pearson.

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shivanisharma1995rocketmail
Posted 8 years ago. Direct link to shivanisharma1995rocketmail's post “What is the significance ...”
What is the significance of the undershoot that happens during the hyper polarization event?Does it serve a specific purpose?
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- William H
  Posted 8 years ago. Direct link to William H's post “Yes, it prevents the acti...”
  Yes, it prevents the action potential from going backwards.
  Comment on William H's post “Yes, it prevents the acti...”
  (16 votes)
Josie G.
Posted 7 years ago. Direct link to Josie G.'s post “What happens if the sodiu...”
What happens if the sodium/potassium pump is nonfunctional and the membrane potential can't return to the resting membrane potential? Can another action potential be produced, or will the membrane potential never be able to reach the threshold again?
Button navigates to signup pageComment on Josie G.'s post “What happens if the sodiu...”
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- jpmartin
  Posted 5 years ago. Direct link to jpmartin's post “Hi, I'm a neurobio profes...”
  Hi, I'm a neurobio professor, and this is one of the biggest misconceptions in neuroscience. The pump plays no direct role in returning to resting potential. The pump simply maintains the concentrations gradients over a long time period.
  But: When an action potential occurs, only a tiny, tiny amount of ions (<0.001%) need to move across the membrane to change the membrane potential. This is because membrane potential changes are not determined by concentration changes, but by permeability changes. The membrane potential is a function of the relative permeability (through ion channels) of the membrane to each ion, and the equilibrium potential (E_ion) for that ion. The E_ion is determined by the concentration gradient set up by the pump. The membrane is hyperpolarized at the end of the AP because voltage-gated potassium channels have increased the permeability to K+. As they close, the membrane returns to the resting potential, which is set by permeability through the "leak" channels. Those are mostly K+ channels, so the membrane potential is still very close to E_K.
  Comment on jpmartin's post “Hi, I'm a neurobio profes...”
  (13 votes)
Jimmy
Posted 8 years ago. Direct link to Jimmy's post “Why does people with one ...”
Why does people with one sort of epilepsy suffer from seizures while others don't? Is it because some sort of abnormality in the membrane potential?
Button navigates to signup pageButton navigates to signup page
(4 votes)
Answer
- Vivian
  Posted 4 years ago. Direct link to Vivian's post “Contrary to these other t...”
  Contrary to these other two answers, I think you're spot on with the mechanistic explanation. Of course, it gets much more complicated if you look into it. Fundamentally, the problem in epilepsy is that some resting membrane potentials in any of the clusters of cells in the brain can move closer to threshold. So, instead of needing to integrate enough excitatory signals to go from -70mv -> -55mV, someone with epilepsy might have a nucleus in the brain (a cluster of cell bodies) that only needs to depolarize from -60mV -> -55mV in order to fire action potentials. Genetic factors can cause this, but certain drugs can cause it as well, such as lamotrigine.
  
  Once this cluster of neurons recieves strong enough stimulus for the activation to spread (the stronger the stimulus, often the more neurons become involved), the entire cluster of neurons can easily depolarize at once, creating the characteristic waves of excitation seen in epilepsy.
  
  For example, in photosensitive epilepsy, intense visual stimuli cause a critical mass of neurons in the visual cortex to fire synchronously, initiating a wave of excitation.
  Button navigates to signup page
  (2 votes)
Justin Liu
Posted 8 years ago. Direct link to Justin Liu's post “How do synapses affect th...”
How do synapses affect the speed with which a nerve impulse is transmitted?
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(4 votes)
Answer
- YEBrandy
  Posted 8 years ago. Direct link to YEBrandy's post “Electrical synapses are p...”
  Electrical synapses are present, but rare- where the synaptic cleft is negligible in length (i.e. impulses can pass directly from the terminal to a dendrite.) They are much more common in invertebrates.
  Comment on YEBrandy's post “Electrical synapses are p...”
  (2 votes)
Mary Bergeron
Posted 5 years ago. Direct link to Mary Bergeron's post “are sodium and potassium ...”
are sodium and potassium gates ever open a the same time during the action potential?
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(3 votes)
Answer
- Ivana - Science trainee
  Posted 5 years ago. Direct link to Ivana - Science trainee's post “As I am informed so far, ...”
  As I am informed so far, there is no such moment during the generation of an action potential. As soon as potassium channels open, before that sodium channels close (repolarization).
  Button navigates to signup page
  (2 votes)
bio fida
Posted 8 years ago. Direct link to bio fida's post “are there any other types...”
are there any other types of neurons? If so then how many
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(2 votes)
Answer
- YEBrandy
  Posted 8 years ago. Direct link to YEBrandy's post “Many different types, bro...”
  Many different types, broadly categorized with respect to their shape or their function. Motor neurons, interneurons (AKA relay neurons) and sensory neurons are the traditional classifications with respect to function. Motor neurons transmit a signal to an 'effector' of some kind (a muscle or a gland perhaps), interneurons transmit signals between surrounding neurons, and sensory neurons 'receive' stimuli (interpreting the stimulus and integrating it).
  Button navigates to signup page
  (2 votes)
amon grace
Posted 4 years ago. Direct link to amon grace's post “if the permeability of ax...”
if the permeability of axon membrane to Na+ and K+ increased simultaneously what effect would this have on the action potential?
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(2 votes)
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Abbysut679
Posted 4 years ago. Direct link to Abbysut679's post “There is a strong inward ...”
There is a strong inward sodium current during the falling phase of the action potential.
Yet, the total membrane current is outward during this time. Why?
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(2 votes)
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- Ivana - Science trainee
  Posted 4 years ago. Direct link to Ivana - Science trainee's post “Because Cl channels open ...”
  Because Cl channels open too so negative inflow might be...
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  (1 vote)
Vanessa Palmer
Posted 5 years ago. Direct link to Vanessa Palmer's post “When would a nicotinic re...”
When would a nicotinic receptor depolarize? Does it hyperpolarize and how does this happen? I dont undertstand the connection between the receptors binding to channels such as nicotinic and muscarinic and how they depolarize or hyperpolarize the cell?
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(2 votes)
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- Ivana - Science trainee
  Posted 4 years ago. Direct link to Ivana - Science trainee's post “At the synapse of a motor...”
  At the synapse of a motor neuron and striated muscle cell, binding of acetylcholine to nicotinic acetylcholine receptors triggers a rapid increase in permeability of the membrane to both Na+ and K+ ions, leading to depolarization, an action potential, and then contraction.
  
  https://www.ncbi.nlm.nih.gov/books/NBK21586/
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  (1 vote)
Raven Tarlengco
Posted 5 years ago. Direct link to Raven Tarlengco's post “What will happen if large...”
What will happen if large amount of neurotransmitters were maintained in the synaptic cleft for longer periods?
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(2 votes)
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- Ivana - Science trainee
  Posted 5 years ago. Direct link to Ivana - Science trainee's post “1. Neurotransmitters cann...”
  1. Neurotransmitters cannot act unless they reach their receptors.
  2. They are not harmful to the extracellular matrix, however, they will tend to diffuse if they can pass through the membrane.
  
  However, I do not find it as easily possible scenario. :D
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  (1 vote)