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Neurons are the cells that make up our nervous
system, and they’re made up of three main
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parts.
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The dendrites, which are little branches off
of the neuron that receive signals from other
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neurons, the soma, or cell body, which has
all of the neuron’s main organelles like
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the nucleus, and the axon which is intermittently
wrapped in fatty myelin.
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Those dendrites receive signals from other
neurons via neurotransmitters, which when
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they bind to receptors on the dendrite act
as a chemical signal.
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That binding opens ion channels that allow
charged ions to flow in and out of the cell,
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converting the chemical signal into an electrical
signal.
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Since a single neuron can have a ton of dendrites
receiving input, if the combined effect of
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multiple dendrites changes the overall charge
of the cell enough, then it triggers an action
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potential- which is an electrical signal that
races down the axon up to 100 meters per second,
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triggering the release of neurotransmitter
on the other end and further relaying the
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signal.
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So neurons use neurotransmitters as a signal
to communicate with each other, but they use
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the action potential to propagate that signal
within the cell.
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Some of these neurons can be very long, especially
ones that go from the spinal cord to the toes,
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so the movement of this electrical signal
is super important!
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But why does the cell have an electric charge
in the first place?
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Well, it’s based on the different concentrations
of ions on the inside versus outside of the
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cell.
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Generally speaking, there are more Na+ or
sodium ions, Cl- or chloride ions, and Ca2+
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or calcium ions on the outside, and more K+
or potassium ion and A- which we just use
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for negatively charged anions, on the inside.
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Overall, the distribution of these ions gives
the cell a net negative charge of close to
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-65 millivolts relative to the outside environment
- this is called the neuron’s resting membrane
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potential.
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When a neurotransmitter binds to a receptor
on the dendrite, a ligand-gated ion channel
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opens up to allow certain ions to flow in,
depending on the channel.
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Ligand-gated literally means that the gate
responds to a ligand, which in this case is
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a neurotransmitter.
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So if we take the example of a ligand-gated
Na+ ion channel, which, when it opens, lets
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Na+ flow into the cell.
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The extra positive charge that flows in makes
the cell less negative (since remember it’s
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usually -65mV), and therefore less “polar”
- so that’s why gaining positive charge
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is called depolarization.
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Neurotransmitters typically open various ligand-gated
ion channels all at once, so ions like sodium
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and calcium, may flow in, while other ions
like potassium, may flow out, which would
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actually mean some positive charge leaves
the cell.
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In the end though - when it’s all added
up - if there is a net influx of positive
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charge, then it’s called an excitatory postsynaptic
potential (EPSP).
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In contrast, the opening of only ligand-gated
Cl- ion channels would cause a net influx
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of negative charge, creating an inhibitory
postsynaptic potential (IPSP), making the
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cell potential more negative or repolarizing
it.
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Now, a single EPSP or IPSP causes only a small
change on the resting membrane potential,
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but, if there are enough EPSPs across multiple
sites on the dendrites then collectively they
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can push the membrane potential to a specific
threshold value- typically about -55mV, although
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this can vary by tissue.
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When this occurs, it triggers the opening
of voltage-gated Na+ channels at the start
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of the axon - the axon hillock, voltage-gated
channels open in response to a change in voltage,
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and when these open sodium to rush into the
cell.
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The influx of sodium ions and the resulting
change in membrane potential causes nearby
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voltage-gated sodium channels to open up as
well - setting off a chain reaction that continues
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down the entire length of the axon—which
is our action potential, and when this happens,
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we say that the neuron has ‘fired.’
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Once a lot of sodium has rushed across the
neuronal membrane, the call actually becomes
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positively charged relative to the external
environment - up to about +40mV.
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The depolarization process ends when the sodium
channel stops allowing sodium to flow into
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the cells- a process known as inactivation.
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But this state is different than when the
channel’s closed, or open for that matter,
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which is what most of the other channels have.
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The voltage-gated sodium channel, though,
is unique in that it has what’s known as
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the inactivation gate, which blocks sodium
influx shortly after depolarization, until
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the cell repolarizes and the channel enters
the closed state again and the inactivation
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gate stops blocking influx, although even
though the inactivation gate’s not blocking,
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the channel’s still closed so no sodium
enters the cell.
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This middle open state therefore is the only
state where sodium gets let into the cell
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through the channel, and this is a very short
window of time.
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Now in addition to these sodium voltage-gated
channels, we’ve also got potassium voltage-gated
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channels, which are slow to respond and don’t
open until the sodium channels have already
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opened and become inactivated.
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The result is that after the initial sodium
rush into the cell, potassium flows out of
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the cell down its own electrochemical gradient-
removing some positive charge and blunting
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the effect of the sodium depolarization.
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The potassium channels, do not have a separate
inactivation gate and therefore remain open
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for slightly longer, which means that there
is a period of time when there is a net movement
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of positive ions out of the cell, causing
the membrane potential to become more negative,
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or repolarize.
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During this repolarization phase, the cell
also relies on the sodium-potassium pump,
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an active transporter that moves three sodiums
out of the cell and two potassiums into it.
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It’s during this repolarization phase that
the cell’s in its absolute refractory period,
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since the sodium channels are inactivated
and won’t respond to any amount of stimuli.
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This absolute refractory period keeps the
action potentials from happening too close
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together in time, but also keeps the action
potential moving in one direction.
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The combined efforts of this pump and the
extended opening of the potassium channels
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results in a small period of overcorrection
where the neuron becomes hyperpolarized relative
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to the resting potential, and at this point
the sodium channels go back to their initial
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closed state, and for a short period the potassium
channels stay open.
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Now we’re in the relative refractory period
since the sodium channels are closed but can
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be activated, but because the potassium channels
are still open and we’re in a hyperpolarized
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state, so it’s takes a strong stimulus to
do so.
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Finally, as the potassium channels close,
the neuron returns to it’s resting membrane
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potential.
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Alright, as a quick graphical recap, with
membrane potential on the y and time on the
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x.
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First we start at resting potential of around
-65 mV and voltage-gated sodium and potassium
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channels are closed, we receive EPSPs enough
to hit threshold at about -55 mV, voltage-gated
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sodium channels open and we reach a peak of
about +40 mV, at which point the sodium channels
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become inactivated and we’re in the absolute
refractory period.
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Voltage-gated potassium channels open, and
along with the sodium-potassium pump, start
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to repolarize the cell, so much so that it
overshoots and hyperpolarizes the cell.
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Next the sodium channels enter their closed
resting state as potassium channels start
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to close we’re in the relative refractory
period, until finally they all close and we
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reach our resting membrane potential.
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Alright, so this process of positive sodium
ions moving in and depolarizing the cell transmits
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the electrical signal down the length of the
axon.
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Great.
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But really, this process isn’t that fast.
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So that’s where the fatty myelin comes in,
which comes from glial cells like Schwann
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cells or oligodendrocytes.
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These myelinated areas don’t have voltage-gated
ion channels spanning the membrane, so ions
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can’t simply flow into the cell, that only
happens in the spots between the myelin, called
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nodes of Ranvier.
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So instead of propagating via channels, the
charge essentially jumps from node to node.
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That said though, these ions aren’t just
diffusing down the length of the myelin to
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the other side...that’d be way to slow.
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What actually happens is more like the sodium
ions rushing in bumps other positive sodium
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ions already inside the cell, which bumps
another one, and so on until it reaches the
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next node.
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The charge moving in this way with the myelinated
areas moves really fast, and is called saltatory
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conduction, which makes it look like the action
potential “jumps” from one one node to
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the next.
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Okay extremely quick recap - neuron action
potentials happen when dendrites receive enough
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EPSPs to open voltage-gated sodium channels,
which cause rapid depolarization of the neuronal
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membrane and propagation of an electrical
charge from node to node down the length of
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the axon.
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