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Current time:0:00Total duration:9:40

Video transcript

in this video I want to talk about neural plasticity neural plasticity refers to how the nervous system changes in response to experience because 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 and we have only a very limited understanding of how this happens that at the level of the cells of the nervous system we know a few things that go along with neural plasticity 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 and 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 refers to kind of depressing the responses of cells to other cells in the nervous system versus potentiating the responses of cells the amount of neural plasticity is highest during development to the nervous system and lower afterward but it's still present throughout life and 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 to grow weaker which we call depression neuroplasticity 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 that's target cell are changed this we could call structural neuroplasticity structural so let's go through a few examples of some of the changes that we know about occurring with neural the city 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 so that here in green will be the axon terminal of these different neurons in 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 so 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 so we'll say that these are all action potentials and there's just lots of action potentials coming down this axon so that this axon terminal is frequently releasing neurotransmitter into the synaptic cleft and frequently stimulating the target cell by lots of neurotransmitter binding to the neurotransmitter receptors on the target cell membrane on the postsynaptic membrane well 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 postsynaptic membrane there may be an increase in the number of neurotransmitter receptors in the postsynaptic 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 on the target cell just because it's much more sensitive to the neurotransmitter that's being released either or these changes from the axon terminal releasing more neurotransmitter or the postsynaptic 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 so that would be synaptic potentiation now there's a lot of research going on trying to understand how these changes occur because it seems like there's communication going both directions from both the axon terminal to the postsynaptic membrane as well as backwards and all the processes for how this is happening I've not been worked out yet now let's consider the opposite let's consider synaptic depression so let's say I draw a little line here to represent time and let's say we're very having very few action potentials just the occasional action potential I'll just show this little spike here and we're just not having much activity we're not having many action potentials reach this axon terminal so 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 so that for each action potential last 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 so that maybe we had more neurotransmitter receptors to begin with and that some of those go away so we have a smaller number of receptors or changes to the receptors to some less responsive kind of receptor or changes to second messengers so that the target cell just doesn't respond as much to any given amount of neurotransmitter so in either of these changes we'd see less of a response in the target cell to an action potential reaching the axon terminal now 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 a neuron and its target cell so we can call structural neural plasticity so for example let's consider a couple of chains of neurons let me draw a couple of neurons in a chain for each each of these examples the potentiation and the depression and let's say they start out looking pretty similar they 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 and 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 will be its target cell in this situation now I'll just draw relax anima target neuron as well so if these two neurons are firing together frequently if this neuron is 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 and we can see that from the dendrites we could see the dendrites getting longer or growing more branches so they become more more complex trees of dendrites or we could see that from this presynaptic neuron it could start sprouting more axon branches and terminals so that it's forming more synaptic connections with the with the dendritic tree over here so with this kind of structural potentiation both of these neurons are sprouting lots more little branches or either sprouting axon terminals or sprouting more dendritic branches so 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 and then 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 lengths of dendrites or losing dendrite branches and the dendritic tree can become simpler and shorter or we may start losing axon terminals we may simplify the axon terminals that are coming out of the axon and if this if this neuron is not firing very often at all we may actually lose this neuron it may actually go away and 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 again just kind of like plants if you're kind of pruning pieces off a plant so that it has less twigs or branches it's the same idea now both potentiation and depression can happen over a wide spectrum of time we often kind of 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 and synaptic neuroplasticity can contribute to both short-term and long-term potentiation or depression and then these structural changes tend to go along with more long term potentiation or depression and I think 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 its wiring itself together based on the experience that the nervous system is receiving during its formative time and also this plays a huge role in memory and learning and recovery from injury to the nervous system when it's kind of trying to wire itself back together after it's been injured so these are a few of the things we we know about neural plasticity but there's a lot more that we don't understand yet and 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 it can change over time