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.
