Tricky Topics: Action Potentials
Summary
TLDRThis script explores how neurons communicate via electrochemical signals, focusing on action potentials. It explains the roles of excitatory and inhibitory postsynaptic potentials in reaching the threshold for an action potential. The video details the process of action potential generation, propagation along the axon, and termination at the axon terminals. It also touches on how substances like novocaine and tetrodotoxin can block sodium channels, affecting action potentials, and how drugs can manipulate neurotransmitter levels to treat conditions like depression and Alzheimer's.
Takeaways
- đ§ Neurons communicate using electrochemical signals, with neurotransmitters playing a key role in transmitting messages across synapses.
- đ Neurons have two main functions: transmitting messages to a target neuron via a synapse and carrying messages along the axon to the next neuron.
- đ Graded potentials, both excitatory (EPSPs) and inhibitory (IPSPs), determine when a neuron reaches the threshold to initiate an action potential.
- ⥠Action potentials are electrical signals generated when the membrane potential reaches a threshold of -55 millivolts, leading to the opening of voltage-gated sodium channels.
- đ Action potentials propagate along the axon to the terminals, with the nervous system operating within a sensitive computational timeframe, some traveling at speeds up to 100 meters per second.
- đĄ Myelin sheaths, formed by glial cells, insulate axons and allow electrical charge to jump between nodes of Ranvier, increasing the speed of action potential propagation.
- đ The action potential involves a cycle of depolarization, caused by sodium influx, and repolarization, caused by potassium efflux, to restore the resting membrane potential.
- đ Local anesthetics like novocaine block sodium channels, preventing the depolarization phase of action potentials, which is essential for nerve signaling.
- đĄ Tetrodotoxin, found in pufferfish, is a potent sodium channel blocker that can be lethal by paralyzing the respiratory system.
- đ When an action potential reaches the axon terminal, it triggers the opening of voltage-dependent calcium channels, which are necessary for neurotransmitter release through exocytosis.
- đ Neurotransmitter release is terminated by either reuptake into the presynaptic neuron or enzymatic degradation in the synaptic cleft.
Q & A
How do neurons communicate with each other?
-Neurons communicate with each other using the language of electrochemistry, primarily through the release of neurotransmitters and the generation of action potentials.
What are the two important jobs of a neuron?
-A neuron's two important jobs are to transmit a message to a target across a synapse and to carry a message along the length of the axon to the next neuron.
What are the two types of postsynaptic potentials?
-The two types of postsynaptic potentials are excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs).
What is the threshold membrane potential that triggers an action potential?
-The threshold membrane potential that triggers an action potential is minus 55 millivolts.
How does the action potential propagate along the axon?
-The action potential propagates along the axon through the sequential opening of voltage-gated sodium channels, which allows sodium ions to rush into the neuron, further depolarizing the membrane.
What is the role of myelin sheaths in the nervous system?
-Myelin sheaths, formed by glial cells, insulate the axons and allow electrical charge to quickly jump between myelin segments, increasing the speed of action potential propagation.
What are nodes of Ranvier and why are they significant?
-Nodes of Ranvier are the spaces between myelin sheaths that are densely clustered with ion channels, allowing the passage of electrical charge across the membrane and facilitating the rapid propagation of action potentials.
What happens when the membrane potential reaches positive 40 millivolts during an action potential?
-When the membrane potential reaches positive 40 millivolts, voltage-gated sodium channels inactivate, and voltage-gated potassium channels open, leading to potassium efflux and the repolarization phase of the action potential.
What is the refractory period and why is it important?
-The refractory period is a brief period of time when the neuron is hyperpolarized and unlikely to fire off another action potential, ensuring that the action potential only travels in one direction.
How do neurons terminate their response after an action potential?
-Neurons terminate their response through two main methods: presynaptic reuptake, which uses transporter proteins to repackage neurotransmitters, and enzymatic degradation, which breaks down neurotransmitters in the synapse.
How do drugs like novocaine work to block action potentials?
-Drugs like novocaine are sodium channel blockers, which prevent the depolarizing phase of action potentials, thus blocking the initiation of action potentials and causing a numbing effect.
What is tetrodotoxin and how does it affect the nervous system?
-Tetrodotoxin is a powerful sodium channel blocker found in pufferfish. It can lead to paralysis and death by blocking action potentials in the respiratory system.
Outlines
đ§ Neuronal Communication and Action Potentials
This paragraph explains the fundamental aspects of neuronal communication, emphasizing the role of neurotransmitters in transmitting messages across synapses and the importance of action potentials for signal transmission along the axon. It details how neurons sum excitatory and inhibitory postsynaptic potentials to determine when to initiate an action potential, which is triggered when the membrane potential reaches a threshold of -55 millivolts. The paragraph also discusses the initial step of an action potential, which involves the opening of voltage-gated sodium channels, and how these channels are distributed along the axon. The movement of sodium ions into the neuron and the subsequent depolarization are described, along with the role of myelin sheaths in increasing the speed of action potentials.
đ The Propagation of Action Potentials
This section delves into the process of how action potentials propagate along the axon towards the neuron's terminals. It explains the role of voltage-gated sodium channels in initiating the action potential and how the influx of sodium ions leads to further depolarization. The paragraph describes the sequential opening of sodium channels along the axon, allowing the depolarization wave to travel towards the terminals. It also discusses the repolarization phase, where voltage-gated potassium channels open, leading to potassium efflux and the return of the membrane potential to its resting state. The refractory period, during which the neuron is temporarily unable to generate another action potential, is also explained.
đ The Cycle of Action Potentials
This paragraph focuses on the cycle of action potentials, starting with the resting membrane potential of a neuron and the threshold for initiating an action potential. It describes the depolarization phase, where sodium influx leads to a positive membrane potential, and the subsequent repolarization phase, where potassium efflux returns the membrane potential to its resting state. The refractory period is also mentioned, ensuring unidirectional propagation of the action potential. The paragraph concludes with a discussion of how neurons restore ion concentrations after an action potential and the role of graded potentials in initiating action potentials.
đ Termination of Neuronal Responses
This section discusses the termination of neuronal responses, which is crucial for the proper functioning of the nervous system. It explains two primary methods of terminating neural transmission: presynaptic reuptake and enzymatic degradation. Presynaptic reuptake involves transporter proteins thatćæ¶neurotransmitters into the presynaptic terminal for reuse, while enzymatic degradation involves the metabolic breakdown of neurotransmitters, rendering them inactive. The paragraph provides examples of drugs that affect these processes, such as SSRIs that block serotonin reuptake to treat depression and Alzheimer's drugs that inhibit the breakdown of acetylcholine to enhance memory signals.
Mindmap
Keywords
đĄNeurons
đĄAction Potentials
đĄVoltage-gated Sodium Channels
đĄNeurotransmitters
đĄGraded Potentials
đĄMyelin Sheaths
đĄNodes of Ranvier
đĄDepolarization
đĄRepolarization
đĄRefractory Period
đĄExocytosis
Highlights
Neurons communicate using electrochemical signals.
Action potentials are crucial for transmitting information over long distances.
Neurotransmitters trigger graded potentials in the postsynaptic neuron.
Graded potentials are either excitatory or inhibitory.
Action potentials are generated when membrane potential reaches threshold.
The axon's main job is to propagate action potentials to the neuron's target.
Voltage-gated sodium channels play a key role in the initiation of action potentials.
Myelin sheaths increase the speed of action potential propagation.
Nodes of Ranvier are areas of high ion channel concentration for electrical charge passage.
Action potentials propagate in a proximal to distal direction along the axon.
Sodium influx through voltage-gated channels is essential for action potential propagation.
Voltage-gated potassium channels contribute to the repolarization phase of action potentials.
The refractory period ensures unidirectional action potential travel.
Special pumps restore ion concentrations after an action potential.
Graded potentials vary in size, unlike action potentials which are all-or-none.
The strength of an action potential is coded by frequency.
Local anesthetics like novocaine block sodium channels to prevent action potentials.
Tetrodotoxin, a poison in pufferfish, is a powerful sodium channel blocker.
When an action potential reaches the axon terminal, it triggers calcium channels for neurotransmitter release.
Neurons terminate responses by reuptake or enzymatic degradation of neurotransmitters.
SSRIs work by blocking serotonin reuptake to treat depression.
Drugs like donepezil boost acetylcholine levels to improve memory in Alzheimer's patients.
Transcripts
[Music]
neurons communicate with each other
using the language of electrochemistry
and to appreciate how information is
transmitted across large distances in
some cases over a meter it's necessary
to understand how action potentials work
but first let's review the basics of
neuronal communication neurons have two
important jobs one is to transmit a
message to a target across a synapse and
the other is to carry a message along
the length of the axon to the next
neuron the first job is made possible by
neurotransmitters released from the
presynaptic neuron they trigger graded
potentials in the postsynaptic neuron
which come in two flavors excitatory
postsynaptic potentials or epsps and
inhibitory postsynaptic potentials or
ipsps the neuron has the ongoing task of
adding up all the epsps
and ipsps to determine when to start the
neuron second job of carrying the
message down the length of its axon if
the membrane potential reaches its
threshold of minus 55 millivolts a type
of electrical signal called an action
potential is generated the action
potential then triggers neurotransmitter
release once it reaches the terminals
and the process starts all over again in
the new neuron
although an action potential is first
generated where the membrane potential
reaches minus 55 millivolts which is
usually in the axon initial segment
right at the soma we'll focus on the
events in the axon since their main job
is to propagate the action potentials to
the neurons target at the terminals the
first step of an action potential is
opening of voltage-gated sodium channels
as a postsynaptic neuron receives
neurotransmitter signals if the
threshold of minus 55 millivolts is
reached a special type of sodium channel
that sensitive to electrical changes
gets opened let's take a quick look at
how different receptor types distribute
in a neuron
unlike the receptor channels in the
synapse that are neurotransmitter gated
that is they open in response to
specific neurotransmitter binding
voltage dependence sodium channels which
are most densely located in the axon
open when the membrane potential is
depolarized to minus 55 millivolts in a
resting neuron there are more sodium
ions outside the neuron than inside so
there's a chemical and electrical
imbalance that promotes sodium movement
inside the cell
thus when voltage dependent sodium
channels open sodium rushes into the
neuron bringing its positive charge
making the sell even more depolarized
once an action potential is initiated it
propagates along the axon to its
terminals if we think about the nervous
system as a whole
hundreds of millions of action
potentials are being fired on top of one
another at all times
thus the nervous system must operate
within a remarkably sensitive
computational timeframe indeed some
action potentials can travel at speeds
of up to a hundred meters per second one
strategy the nervous system uses to
increase action potential speed to as
quick as possible is the surrounding of
axon shafts with the fatty membranes of
glia cells
in the central nervous system
oligodendrocytes form fatty myelin
sheaths along axons as seen here this
insulates the axon allowing electrical
charge to quickly jump between myelin
within the axon the space between the
myelin sheaths are referred to as nodes
of ranvier if we zoom in into a node of
ranvier we see that this area is densely
clustered with ion channels which allow
the passage of electrical charge in the
form of ions across the membrane in
areas not covered by the myelin let's
now take a closer look at the mechanisms
behind an action potentials travel down
the axon away from the soma to the axon
terminals here we can see a neuron with
its axon extending away from its soma if
we take a cross-section along the length
of its axon and zoom in we can start to
appreciate what's happening inside the
neurons axon when the graded potentials
at the synapse add up to minus 55
millivolts this is detected by the
voltage dependent sodium channels which
are found in large numbers along the
axon as the voltage-gated sodium
channels open sodium rushes into the
axon along its electrochemical gradient
bringing its positive charge into the
neuron this depolarization is then
sensed by neighboring sodium channels
which also open when the membrane
potential reaches minus 55 millivolts
having sodium ions and positive charged
rush into the neighboring region of the
axial
at this time point if we were to stick
an electrode into the neuron we would
see the membrane potential rise at the
location where the sodium channels are
opening at this time point this location
is proximal to the soma that is it is
closer to the soma than the terminals
the wave of depolarization makes its way
down the axon as neighboring sodium
channels along each part of the axon
open allowing sodium to continue to flow
in
this depolarization wave travels in a
proximal to the stalled direction at a
time point - if we were to again stick
an electrode into the neuron the
depolarization would be measured farther
down the axon this process of sodium
channels bringing positive charge which
then opens adjacent voltage dependent
sodium channels works its way
uninterrupted
all the way down the length of the axon
so once an action potential gets started
it doesn't stop until it runs out of
neuron
while voltage-gated sodium influx is a
key mechanism of action potential
propagation it is only half the story
let's return to where we started at the
beginning of the axon in review when the
neuron is depolarized to minus 55
millivolts from graded potentials
voltage-gated sodium channels open this
allows sodium to travel across its
electrochemical gradient from outside
the neuron to inside the neuron this
causes a further depolarization of the
neuron to positive 40 millivolts when
the membrane potential reaches positive
40 millivolts two things happen one
voltage dependent sodium channels
inactivate and two voltage dependent
potassium channels open keep in mind
that potassium is more concentrated
inside the neuron so when its channel
opens its concentration difference is a
driving force for potassium movement
outside the neuron at a membrane
potential of positive 40 millivolts
there is also an electrical reason for
potassium to leave the neuron when
positively charged potassium leaves the
neuron it brings its positive charge
outside the neuron with it which makes
the membrane potential inside more
negative and helps to balance the charge
difference of the sodium influx let's
come back to the electrical voltage
recording of the axon at time point 1 if
we zoom in we can notice there are two
main components of the action potential
first when the cell reaches minus 55
millivolts it triggers an exponential
rise in the membrane potential to
positive 40 millivolts this rise is a
product of sodium influx through
voltage-gated sodium channels
once the action potential reaches
positive 40 millivolts its second
component can be seen the membrane
potential falls back to its negative
resting membrane potential this is due
to the closing of voltage-gated sodium
channels and more importantly the
opening of voltage-gated potassium
channels which allow the potassium
efflux out of the neuron this is the
repolarizing phase of the action
potential so if we come back to watch
our action potential travel down the
axon at each step along the axon
voltage-gated sodium channels open
followed by voltage-gated potassium
channels
understanding the voltage changes across
the membrane as the action potential
moves down the axon is essential to
understanding its propagation mechanisms
so let's again review the changes across
the membrane during an action potential
except one step closer at rest when the
neuron is not receiving any input its
membrane potential is at about minus 70
millivolts all the voltage-gated sodium
and voltage-gated potassium channels are
closed such that very few sodium ions
and very few potassium ions are moving
across the membrane if the neuron gets
enough excitatory postsynaptic
potentials and not too many inhibitory
postsynaptic potentials it will reach
the threshold of minus 55 millivolts and
the voltage dependent sodium channels
will open allowing for sodium influx
this is called the depolarization phase
which is the part of the action
potential where the membrane potential
climbs all the way to positive 40
millivolts a positive 40 millivolts the
sodium channels deactivate and the
voltage dependent potassium channels
open potassium leaves the neuron along
its electrochemical gradient taking its
positive charge with it this is called
the repolarization phase since the
membrane potential returns back to minus
70 millivolts for a brief period of time
potassium keeps moving out of the cell
hyperpolarizing the neuron so it sits at
less than minus 70 millivolts which
ensures that this segment of the axon
will be unlikely to fire off another
action potential this is called the
refractory period and ensures that the
action potential only travels in one
direction
finally once the action potential is
finished at a certain region of the axon
the neuron uses special pumps to restore
the ions to their regional
concentrations and only then is that
segment of the axon ready to fire again
let's put this all together by
considering a snapshot that captures all
the voltage changes over the duration of
an action potential from beginning to
end keep in mind that this is happening
all over the neuron but we're just
looking at one small segment of the axon
first let's focus in on graded
potentials which lead to action
potential initiation
however unlike action potentials which
are all or none graded potentials vary
in size as shown here graded potentials
can lead to different sizes of
depolarization or hyperpolarization x'
in contrast action potentials happen the
same way every time they're triggered so
the strength of an action potential is
coded by frequency or the number of
action potentials per time period a
strong signal will produce more action
potentials than a weaker one over the
same period of time our knowledge of how
ions work to generate action potentials
has allowed us to manipulate the process
to our advantage let's focus on the
depolarizing phase which is strongly
dependent on voltage dependence sodium
channels when the sodium channels open
sodium rushes into the cell kicking off
the whole process so what happens if
these channels are blocked so you need
to have dental work done that requires
drilling not a pleasant experience for
most people most dentists give an
injection of a drug like novocaine the
dead-end sensations in the mouth indeed
most local anesthetics used in dentistry
are sodium channel blockers which means
they prevent the depolarizing phase so
an action potential can't happen
an interesting fact is that drugs like
novocaine were originally derived from
cocaine which is one of the only few
naturally-occurring local anesthetics
part of the cocaine molecule acts as a
sodium channel blocker so it produces a
numbing feeling if rubbed on the gums by
modifying the cocaine molecule
scientists were able to keep the sodium
channel blocker activity but remove the
parts of the molecule that promoted
addictive behavior
how about this cartoon fish what does it
have to do with action potentials this
is the pufferfish which contains a
poison called tetrodotoxin concentrated
in certain organs like the ovaries and
the liver pufferfish can kill you lots
of ways if threatened by a predator they
may puff up which is how it got its name
you can actually die from eating certain
body parts of the puffer fish that
contain tetrodotoxin tetrodotoxin is a
powerful sodium channel blocker and even
tiny amounts can lead to paralysis and
death by blocking action potentials in
the respiratory system so far we have
discussed how an action potential is
initiated and then how it propagates
down the axon however what we haven't
discussed yet is what happens when an
action potential reaches the axon
terminal once an action potential
arrives at the terminal the depolarizing
wave opens up another type of channel
the voltage-dependent calcium channel
like sodium calcium is more concentrated
outside the neuron driving its movement
inside the neuron calcium is necessary
for neurotransmitter release through a
process called exocytosis where the pre
synaptic vesicle fuses with the terminal
membrane to release its contents into
the synapse now it's important that
neurons are responding in a
time-dependent manner so that their
activity is connected to the tasks we're
trying to accomplish for example if I
were to tell you right now to think of
your first-ever teacher you probably
didn't activate that memory until I
asked you to at some point before the
end of this video you'll probably stop
thinking about your first teacher so
your memory neurons turn on and off when
they are needed just as it is important
to initiate a neurons response it's as
important for neurons to terminate that
response when the job is done
there are two main methods to terminate
a neuronal response and they both
involve removing excess
neurotransmitters from the synaptic
cleft
the first way neurons terminate neural
transmission is by presynaptic reuptake
which uses specialized transporter
proteins that span the presynaptic
terminal membrane these transporters
relocate the neurotransmitter molecules
so that they can be repackaged into
synaptic vesicles and used again at a
later time drugs like SSRIs used to
treat depression work by blocking the
reuptake transporters for the
neurotransmitter serotonin allowing it
to hang around in the synapse for a
little longer low serotonin has been
implicated in depression symptoms so by
elevating its levels in the synapse
these drugs attempt to treat the
disorder
the second way neurons terminate neural
transmission is by enzymatic degradation
enzymatic degradation is the metabolic
breakdown of neurotransmitters in the
synapse you can think of it as the
neurotransmitters essentially being
eaten up so they no longer have
biological activity a great drug example
that takes advantage of enzymatic
degradation in the synapse is the
Alzheimer's drug den episode this drug
blocks the breakdown of the
neurotransmitter acetylcholine which is
reduced in the brains of Alzheimer's
patients this allows it to hang around
in the synapse longer and boost memory
signals that decline with the disease
taken together the action potential is
perhaps the most quintessential process
of the nervous system it is responsible
for transporting signals around the
nervous system and remarkably fast times
amazingly humans as well as other
animals like the pufferfish have figured
out ways to alter aspects of the action
potential hijacking the signaling of our
nervous system
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you
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