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