Voiceover: In this video
I want to talk about neuroplasticity.
Neuroplasticity refers to how the nervous
system changes in response to experience.
The nervous system isn't set in stone.
It's constantly changing,
for instance when we form new memories
or when we learn new things.
We have only a very limited understanding
of how this happens.
At the level of the cells of the nervous system
we know a few things that go along with neuroplasticity.
One way to define this term is that it
refers to changes in synapses and/or other
parts of neurons that affect how information
is processed and transmitted in the nervous system.
Neuroplasticity goes in both directions.
The strength of information flowing through
a particular part of the nervous system can
increase, which we call potentiation.
Potentiation or the strength of information flowing through
parts of the nervous system can decrease,
which we call depression.
Depression.
The use of the word depression in this context
shouldn't be confused with the emotional state
of depression or the psychiatric disorder of depression.
Here it refers to depressing the responses of cells
to other cells in the nervous system versus
potentiating the responses of cells.
The amount of neuroplasticity is highest during
development of the nervous system and
lower afterward.
It's still present throughout life.
It transiently increases following
nervous system injury.
Parts of neurons and chains of neurons that
are used often grow stronger meaning that
each action potential will have a larger
effect on the target cell which we call potentiation.
Parts of neurons and chains of neurons that
are used rarely grow weaker, which we call depression.
Neuorplasticity can happen at the synapse,
which we can call synaptic neuroplasticity.
Synaptic neuroplasticity.
Or neuroplasticity can occur at the level of entire cells
where the total number of synapses between a neuron
and its target cell are changed.
This we could call structural neuroplasticity.
Structural.
Let's go through a few examples of some of the changes
that we know about occurring with neuroplasticity.
First, if we look at synaptic neuroplasticity,
let's look at an individual synapse that's
seeing a lot of activity and another
synapse that's not seeing much activity.
Here in green will be the axon terminal
of these different neurons.
Here in light blue will be the target
cell membrane seeing a corresponding
amount of activity from the axon terminal
that it's synapsing with.
For this synapse that's seeing a lot of activity,
let me just draw a little line for time and
a bunch of little spikes representing action potentials.
We'll say that these are all action potentials.
There's just lots of action potentials coming
down this axon.
This axon terminal is frequently releasing
neurotransmitter into the synaptic cleft
and frequently stimulating the target cell
by lots of neurtransmitter binding to the
neurotransmitter receptors on the target cell
membrane, on the post-synaptic membrane.
Several changes can happen at the level of
this individual synapse for synaptic
neuroplasticity that are potentiation meaning
that each individual action potential will
start to elicit a larger response in the target cell.
One change that can occur is that for each
action potential reaching the axon terminal,
more neurotransmitter may be released into
the synapse so that a bigger response is going
to be seen in the target cell because more
neurotransmitter is released from the axon
terminal with each action potential coming down the axon.
Or the change may occur on the post-synaptic membrane.
Ther may be an increase in the number of
neurotransmitter receptors in the post-synaptic
membrane or changes to the types of
neurotransmitter receptors or the responses
that occur through second messengers so that
for any given amount of neurotransmitter
that's released from the axon terminal from
one action potential, a bigger response is seen
in the target cell just because it's much
more sensitive to the neurotransmitter that's
being released.
Either or of these changes from the axon terminal
releasing more neurotransmitter or the
post-synaptic membrane becoming more
responsive, we're going to see an increased
response in the target cell per action
potential that's reaching the axon terminal.
That would be synaptic potentiation.
There's a lot of research going on trying
to understand how these changes occur.
It seems like there's communication going
both directions from both the axon terminal
to the post-synaptic membrane as well as backwards.
All the processes for this is happening
have not been worked out yet.
Now let's consider the opposite.
Let's consider synaptic depression.
Let's say I draw a little line here
to represent time.
Let's say we're having very few action
potentials, just the occasional action potential.
I'll just show this little spike here.
We're just not having much activity.
We're not having many action potentials
reach this axon terminal.
Basically the opposite responses that
can happen with synaptic potentiation with
synaptic depression, we may see that the
amount of neurotransmitter released
from the axon terminal decreases per
action potential.
For each action potential less neurotransmitter
is released into the synaptic cleft.
Therefore there'll be less of a response
in the target cell, and/or we could see that
the neurotransmitter receptors may decrease in number.
Maybe we had more neurotransmitter receptors
to begin with and that some of those go away.
We have a smaller number of receptors or
changes to the receptors to some less
responsive receptor, or changes to second
messengers, so that the target cell just doesn't
respond as much to any given amount
of neurotransmitter.
With either of these changes, we'd see
less of a response in the target cell to
an action potential reaching the axon terminal.
In addition to these changes at the level of
individual synapses with synaptic neuroplasticity,
we can also see changes in the total number
of synapses between the neuron and its target cell
that we can call structural neuroplasticity.
For example let's consider a couple of chains of neurons.
Let me draw a couple of neurons in a chain
for each of these examples, the potentiation
and the depression.
Let's say they start out looking pretty similar.
They both have about the same amount of
dendritic branches and the length of their
dendrites are about the same.
I'll just leave the dendrites off this one.
We'll say that we have about the same
number of axon terminals coming out
and forming synapses between this neuron
and this other neuron which'll be its
target cell in this situation.
I'll just draw a little axon and the target neuron as well.
If these two neurons are firing together frequently;
if this neuron firing lots of action potentials
and this neuron is firing lots of action
potentials in response to this neuron
stimulating it, we can see an increase
in the number of synapses between these two.
We can see that from the dendrites.
We can see the dendrites getting longer or
growing more branches so they become more
complex trees of dendrites.
Or we could see from this pre-synaptic neuron
it could start sprouting more axon branches
and terminals so that it's forming more synaptic
connections with the dendritic tree over here.
With this structural potentiation, both
of these neurons are sprouting lots more
little branches or sprouting axon terminals
or sprouting more dendritic branches.
I'll just write that down here, that we're doing lots of sprouting.
Just like plants may sprout lots of new
shoots in the spring.
The opposite may occur here.
If we're not having very many action
potentials being fired by this neuron
or by this neuron and particularly if they're
not firing action potentials together,
we can see the opposite where we actually
start losing length of dendrites or losing
dendrite branches.
The dendritic tree can become simpler and shorter.
We may start losing axon terminals.
We may simplify the axon terminals that are coming
out of the axon.
If this neuron is not firing very often at all,
we may actually lose this neuron.
It may actually go away.
This type of structural depression where
we're actually losing parts of neurons or entire neurons
because they're not very active, we call pruning.
Just like plants, if you're pruning pieces
off a plant so that it has less twigs or
branches, it's the same idea.
Both potentiation and depression can happen
over a wide spectrum of time.
We often divvy it up into short term changes
such as on the order of seconds or minutes
or long term changes that can be months, years,
or even decades.
Synaptic neuroplasticity can contribute to
both short term and long term potentiation
or depression.
The structural changes tend to go along with
more long term potentiation or depression.
You could imagine how by changing the
strength of information flow through individual
synapses or between cells, by changing the
total number of synapses that there are that
neuroplasticity can play a very important
role in development of the nervous system as
it's wiring itself together based on the
experience that the nervous system is receiving
during its formative time.
Also this plays a huge role in memory and
learning and recovery from injury to the
nervous system when it's trying to wire
itself back together after it's been injured.
These are a few of the things we know
about neuroplasticity.
There's a lot more that we don't understand yet.
There's still a lot of research going on
trying to understand how all these processes happen
and how they contribute to all these amazing
functions of the nervous system that can
change over time.