Neuroplasticity | Nervous system physiology | NCLEX-RN | Khan Academy
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Neuroplasticity | Nervous system physiology | NCLEX-RN | Khan Academy


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.

About James Carlton

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29 thoughts on “Neuroplasticity | Nervous system physiology | NCLEX-RN | Khan Academy

  1. I am thinking that, even if the discovery of neuroplasticity is something very interesting and potentially useful, is not something we already knew from experience? If we stop seeing a person, our feeling of connection with him or her diminish with time. The same if we stay long without practice tennis, we loose abilities. 

  2. Neuroplasticity, also known as brain plasticity, is an umbrella term that encompasses both synaptic plasticity and non-synaptic plasticity—it refers to changes in neural pathways and synapses due to changes in behavior, environment, neural processes, thinking, and emotions – as well as to changes resulting from bodily injury.[1] The concept of neuroplasticity has replaced the formerly-held position that the brain is a physiologically static organ, and explores how – and in which ways – the brain changes in the course of a lifetime.[2]
    Neuroplasticity occurs on a variety of levels, ranging from cellular changes (due to learning) to large-scale changes involved in cortical remapping in response to injury. The role of neuroplasticity is widely recognized[by whom?] in healthy development, learning, memory, and recovery from brain damage. During most of the 20th century, neuroscientists maintained a scientific consensus that brain structure was relatively immutable after a critical period during early childhood. This belief has been challenged by findings revealing that many aspects of the brain remain plastic even into adulthood.[3]
    Hubel and Wiesel had demonstrated that ocular dominance columns in the lowest neocortical visual area, V1, remained largely immutable after the critical period in development.[4] Researchers also studied critical periods with respect to language; the resulting data suggested that sensory pathways were fixed after the critical period. However, studies determined that environmental changes could alter behavior and cognition by modifying connections between existing neurons and via neurogenesis in the hippocampus and in other parts of the brain, including in the cerebellum.[5]
    Decades of research[6] have shown that substantial changes occur in the lowest neocortical processing areas, and that these changes can profoundly alter the pattern of neuronal activation in response to experience. Neuroscientific research indicates that experience can actually change both the brain's physical structure (anatomy) and functional organization (physiology). As of 2014 neuroscientists are engaged in a reconciliation of critical-period studies (demonstrating the immutability of the brain after development) with the more recent research showing how the brain can, and does, change in response to hitherto unsuspected stimuli.[7][8]

  3. @JackVegas Tv: black backgrounds are said to be more "restful" for the eye and have been recommended for slideshows as a result (there was a TED talk on this).

  4. Are NEW STRUCTURAL SYNAPSES actually CREATED when we change or alter thought habits and experiences or are we BORN with all the neural pathways already and simply by changing brain habits and experiences are we merely UTILIZING already EXISTING neural pathways? Do we just access neural pathways that are already there or do new thoughts and experiences actually CREATE new neural pathways?

    Depending upon the answer to the above question, then if a neuroscientist were to be looking at a brain scan or an autopsied brain, would she see all the neural pathways that both had already been utilized as well as the ones that were never used?

  5. Hello, I'm a medical engineering student and I want to do my dissertation on the analysis of neuroplastic changes in the brain when learning. This sort of information is exactly the background I want to learn, can you make more of these videos? Also did you get this info from a book? If so what book? Can anyone recommend any books on neuroplasticity and synaptogenesis?

  6. There are actually how many types of neuroplasticity? cause i found something that is functional plasticity and reparative plasticity

  7. This is a very incredible organ. That is why psychology in my opinion has left out some variables that play into diagnosing actual mental illness that is purely physiological- because beliefs that were ingrained especially in early childhood, whether true or false, play into what we become like in adulthood. So some people may be diagnosed as mentally ill or emotionally unstable- lets use a mood disorder for example: Its important I suppose to ask, "Is this purely physiological and can it be fixed with just medication, or is it a divided mind (our thoughts are very closely tied to emotions) so if a person seems to have many mood swings then it may be that at an hour ago they may have been thinking thoughts condusive to a positive mood, vs an hour later a minir experience (possible misread situation with another person) could lead them into a pattern of thought that creates a negative corresponding emotion. Paranoia is often created out of experiences from my experience that reinforce often false suspicions. Some suspicions and distrust is warranted from some people yet if a individual has gotten so hosed up to the degree their negative life experiences have created a trigger that could set an alarm off to anything they remotly associate with a (negative feeling they have, insecurity or emotion)

  8. This is a very incredible organ. That is why psychology in my opinion has left out some variables that play into diagnosing actual mental illness that is purely physiological- because beliefs that were ingrained especially in early childhood, whether true or false, play into what we become like in adulthood. So some people may be diagnosed as mentally ill or emotionally unstable- lets use a mood disorder for example: Its important I suppose to ask, "Is this purely physiological and can it be fixed with just medication, or is it a divided mind (our thoughts are very closely tied to emotions) so if a person seems to have many mood swings then it may be that at an hour ago they may have been thinking thoughts condusive to a positive mood, vs an hour later a minir experience (possible misread situation with another person) could lead them into a pattern of thought that creates a negative corresponding emotion. Paranoia is often created out of experiences from my experience that reinforce often false suspicions. Some suspicions and distrust is warranted from some people yet if a individual has gotten so hosed up to the degree their negative life experiences have created a trigger that could set an alarm off to anything they remotly associate with a (negative feeling they have, insecurity or emotion)

  9. Thank you for the clear demonstration! I've been so confused with the difference between these two

    Check out NPAS4 gene 🙂 my lab's been working on it and it seems to have an important role in regulating neuroplasticity – both during experience-dependent learning and after injury (particularly stroke)

  10. This explains a lot what's going in my brain rebuilding itself after Benzo Withdrawal. What a hell time of my LIFE 😤😟😨

  11. why would one not correlate depression as a state with depression as the decrease of information or communication between neurons? it would seem that the two would be directly correlated

  12. very interesting!! important for the general public to know. so many frustrations in life come from bad habits that are rationalized with outside factors. if we think emprically, we'll be successful and happy!

  13. i'm a pharmasist and my graduation project is about dopamine and it's connection with addiction and there's alot of neuroplasticity in every thing i read and i needed this video to understand more about brain and connection and how drugs can make changes to the synapses and cause addiction.so thanks alot .. please make more vedios about this 🤓❤ and if u can advice me with some books or websites about that i would be very thankful…

  14. I am suffering from a Lexapro withdrawal and have been kindled with many failed reinstaments. Is there hope for me?

  15. Nice video. Here is almost a FREE CERTIFIED course in Neuroplasticity. https://www.udemy.com/course/neuroplasticity-brain-plasticity-therapy-rewiring-brain-made-easy/

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