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Khan Academy

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Information processing model: Sensory, working, and long term memory

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Learn about the information processing model of human memory.

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Khan Academy

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We all know that our memories aren't perfect. As frustrating as it can be, we forget people's names, birthdays, and other things we'd like to remember. One reason forgetting happens is the very normal process of decay. When we don't encode something well or when we don't retrieve it for a long time, we become unable to retrieve it later. One theory about why this happens is that the pathway to and from the memory, meaning the neural connections between the cues and the memory, become weaker over a period of disuse, so it becomes harder to stimulate those neurons. This is sort of the classic use it or lose it problem. If you learned something once and don't ever revisit the memory, it's likely to decay over time. One interesting pattern of decay is that it seems pretty consistent, even for different types of materials. Your initial rate of forgetting is very high, but it levels off after a period of time. Back in the late 1800s, a German philosopher and psychologist named Ebbinghaus was the first person to really look at the decay in human memory. He made himself learn a bunch of three-letter nonsense syllables, and then he tested himself to see how much he remembered at different time intervals, from zero to 30 days. He found that his rate of forgetting was very rapid at first. If he remembered those words after a few days, however, then he generally remembered them for all 30 days. Later on, people replicated this pattern with different materials and over different time intervals. And they found that the more integrated the initial learning is, the more stretched out the rate of forgetting is, but it's still follows the same pattern. For example, if you study a language for a few years, then it'll take you more than a few days to forget it. Similar to Ebbinghaus's original forgetting curve, though, most of your forgetting will occur within the first few years of disuse. After that point, your forgetting will pretty much level off. The interesting thing about decay and forgetting is that just because you can't retrieve something doesn't mean it's completely gone from your long-term memory. Other than outright retrieval, one way we can tell if people have learned something before is by how quickly they re-learn that information or skill. So remember Ebbinghaus? In addition to forgetting, he studied re-learning with those same three-letter nonsense syllables. He found that even if he couldn't produce all the syllables from his list, it took him less time to learn the list the second time around than the first time, indicating that some foundation of the memory still existed, even though he couldn't produce it at the time. This foundation is called savings, because it's what saved in your memory, whether you realize it or not Re-learning works with procedural skills, too. For example, imagine that you learned how to play particular song on the piano a few months ago, but you can't play any of it today. Now I give you the music to that song and ask you to learn it again. If the inability to retrieve something meant that it was completely gone from your long term memory, then it would take you the same amount of time to learn the song the second time around. However it probably would take you less time to re-learn it than it did for you to learn it originally. This faster rate of re-learning tells us that you still have some information about that song stored in your long-term memory. Sometimes decay isn't the problem, though. It's that something else seems to be blocking our ability to get to the information we want. This experience is called interference, and there are two main types-- retroactive and proactive. Retroactive interference is interference that goes backwards, that is, some new piece of learning seems to reach back and impair your ability to retrieve something you used to know. For example, when you move to a new place, you get used to writing your new address on all the different forms and documents and stuff. And after a while of using this new address, you may find it difficult to recall your old one. In this case, your new address would be running some retroactive interference on your old address Proactive interference, on the other hand, is interference acting forward. Something you learned in the past gets in the way of your ability to learn and retrieve something correctly in the future. So I'll give you an example of something that happened to me a few months ago. I used one password for my email for a really long time. But then I had to change it. Sometimes when I log in, it's still hard for me to remember what my new password is, because all I can come up with is my old one. In this case, the prior learning up my old password is impeding my ability to remember the new one.

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Decay and interference (video) | Memory | Khan Academy

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We all know that our memories aren't perfect. As frustrating as it can be, we forget people's names, birthdays, and other things we'd like to remember. One reason forgetting happens is the very normal process of decay. When we don't encode something well or when we don't retrieve it for a long time, we become unable to retrieve it later.

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Huntington's Disease: Stages and Therapies

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Huntington's Disease: Stages and Therapies

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ADHD As A Difference In Cognition, Not A Disorder: Stephen Tonti at TEDxCMU

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YouTube

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Robert Stickgold

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Long-term Potentiation and Long-term Depression 

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Long-term Potentiation and Long-term Depression 

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Leonard White

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From the course by Duke University

This Course

Video Transcript

Medical Neuroscience explores the functional organization and neurophysiology of the human central nervous system, while providing a neurobiological framework for understanding human behavior. In this course, you will discover the organization of the neural systems in the brain and spinal cord that mediate sensation, motivate bodily action, and integrate sensorimotor signals with memory, emotion and related faculties of cognition. The overall goal of this course is to provide the foundation for understanding the impairments of sensation, action and cognition that accompany injury, disease or dysfunction in the central nervous system. The course will build upon knowledge acquired through prior studies of cell and molecular biology, general physiology and human anatomy, as we focus primarily on the central nervous system. This online course is designed to include all of the core concepts in neurophysiology and clinical neuroanatomy that would be presented in most first-year neuroscience courses in schools of medicine. However, there are some topics (e.g., biological psychiatry) and several learning experiences (e.g., hands-on brain dissection) that we provide in the corresponding course offered in the Duke University School of Medicine on campus that we are not attempting to reproduce in Medical Neuroscience online. Nevertheless, our aim is to faithfully present in scope and rigor a medical school caliber course experience. This course comprises six units of content organized into 12 weeks, with an additional week for a comprehensive final exam: - Unit 1 Neuroanatomy (weeks 1-2). This unit covers the surface anatomy of the human brain, its internal structure, and the overall organization of sensory and motor systems in the brainstem and spinal cord. - Unit 2 Neural signaling (weeks 3-4). This unit addresses the fundamental mechanisms of neuronal excitability, signal generation and propagation, synaptic transmission, post synaptic mechanisms of signal integration, and neural plasticity. - Unit 3 Sensory systems (weeks 5-7). Here, you will learn the overall organization and function of the sensory systems that contribute to our sense of self relative to the world around us: somatic sensory systems, proprioception, vision, audition, and balance senses. - Unit 4 Motor systems (weeks 8-9). In this unit, we will examine the organization and function of the brain and spinal mechanisms that govern bodily movement. - Unit 5 Brain Development (week 10). Next, we turn our attention to the neurobiological mechanisms for building the nervous system in embryonic development and in early postnatal life; we will also consider how the brain changes across the lifespan. - Unit 6 Cognition (weeks 11-12). The course concludes with a survey of the association systems of the cerebral hemispheres, with an emphasis on cortical networks that integrate perception, memory and emotion in organizing behavior and planning for the future; we will also consider brain systems for maintaining homeostasis and regulating brain state.

Neural Signaling: Synaptic Transmission and Synaptic Plasticity

Let's continue our studies of neural signaling by learning about what happens at synaptic junctions, where the terminal ending of one neuron meets a complementary process of another excitable cell.

Meet the Instructors

Associate Professor
Department of Neurology, Department of Neurobiology, Duke University School of Medicine; Department of Psychology & Neuroscience, Trinity College of Arts & Sciences; Director of Education, Duke Institute for Brain Sciences; Duke University

Welcome to this tutorial. This is the first of three devoted to the

fascinating topic of synaptic plasticity. in this tutorial, we're going to talk

about two particular mechanics, one called long-term potentiation or LTP for

short, and the other, long-term depression, LTD.

This tutorial will be followed by one that will frame up our understanding of

plasticity as is occurs in real brains one spike at a time.

And then, lastly, we'll talk about the famous Hebb's postulate and how our

understanding of synaptic plasticity is framed up In those terms.

Well, this topic relates to several key concepts in the field of neuroscience and

they are enumerated below. neuroscience core concepts 2, 4, and 8.

We will continue to talk about how neurons communicate through both

electrical and chemical signals. And the plasticity that we'll be speaking

of in this tutorial relates to plasticity of chemical signaling.

And the point of plasticity is that it provides us with a means for life

experience to change the nervous system. So we're beginning to talk about some of

those most fascinating topics in the field of neuroscience.

Those topics that pertain to understanding how the experiences of our

lives are transduced into permanent change in the nervous system.

All of this holds great promise for the future, fundamental discoveries promote

healthy living and the treatment of disease.

These topics that we will be exploring in the next few sessions are really giving

us a glimpse into the future of medical neuroscience as principles of synaptic

plasticity are better understood. So can rational intervention be developed

that will harness this amazing plastic potential of the central nervous system

for therapeutic advantage. And for those of you that are getting

into the healthcare industries these are exciting times.

Because, as basic neuroscience progresses and this domain of understanding these

principles, so will our capacity to apply these principles for therapeutic good for

the patients that you'll come to serve. So, I'm privileged to be a small part of

your education that will usher in this new frontier in the world of medical

neuroscience, where we will understand how to optimize our capacity to change

the nervous system of someone who is dealing with impairment or disease or

disability. Or, perhaps someone without those

conditions who wants to optimize their performance and whatever domain of life

is of concern to them. So, that's what's possible.

over the course of your lifetime in your practice, as we come to better understand

the brain basis of synaptic change. So I do have some learning objectives for

you. I want you to be able to characterize

general cellular mechanisms for synaptic change.

In particular, I want you to be able to discuss the mechanisms of long-term

potentiation. And I want you to focus on two glutamate

receptors. The AMPA or AMPA, subtype of glutamate

receptor and the NMDA glutamate receptor. And I want you to discuss the role of

these receptors in the induction and maintenance in the induction and

maintenance of long-term potentiation. Likewise, I want you to characterize

long-term depression, and I want you to discuss the molecular basis for long-term

depression in two important regions of the central nervous system, the cerebral

cortex and the cerebellar cortex. Well, you may not need any motivation at

all when it comes to this topic of synaptic plasticity, but again, for those

of you that are pursuing careers in healthcare I think it is especially

pertinent that you learn these lessons well.

one motivating statement, at least for me, has come from one of my colleagues at

Emory University who's been a leading thinker and researcher in the translation

of basic science discovery in the domain of synaptic plasticity to intervention

with people that are dealing with neurological disability.

So what Taub and his colleagues have written some years ago in a really

excellent review, in Nature Reviews Neuroscience, he wrote that behavior,

that is the sensory and motor experiences of our bodies, can have a profound

influence on the function and organization of the nervous system...

And that this effect can be manipulated to therapeutic advantage in individuals

with central nervous system injury. So understanding the rules of plasticity

will increase our capacity to help people that are dealing with central nervous

system injury and disease. Because, we will better understand how to

take the sensory and motor experiences of their own bodies use that capacity to

reshape the structure and function of their nervous systems.

So let's begin this discussion by making sure we really know what we're talking

about when we use this word, plasticity. Plasticity simply means the capacity of

the nervous system to change. And, we can think about this concept from

a number of different perspectives, and I'd like to suggest a few of them.

I'd like to suggest the temperal frame of understanding plasticity.

Plasticity can be short-term. Over the course of milliseconds to

hundreds of milliseconds to seconds to minutes.

It can be long-term. It can last minutes to hours to days to

even a lifetime. Just think back for a moment to some of

your earliest childhood memories. It's amazing is it not that that is even

possible? That some formative event changed the

function, maybe even the structure of your nervous system, in such a way that

those events can be recalled. now years later, in my case decades

later. truly a remarkable achievement for a

nervous system to have this capacity to store a lifetime of change.

Now, of course, that's not to say that the process of remembering or recalling

does not, itself, induce a new round of plasticity, indeed it doe But

nevertheless, the basic information that was laid down in the initial event that

you and I may be recalling. is still with us.

It's still present in the functional architecture of our brains.

Amazing. So, our discussion today will begin to

get at an explanation as to what may have changed and how w can also consider

plasticity in spacial terms. That is, where does plasticity occur?

Well, plasticity occurs at synapses. That's what we will talk about today.

Plasticity might also occur within the structure and function of the neuron

itself. That is, it may simply not be a change at

the synapse, but perhaps a change in different compartments within the neuron

and the same could be said of glial cells.

And in particular, I'm thinking about astrocytes that are important in

modulating the activities of neurons within grey matter.

Astrocytes themselves are subject to plastic responses induced by changes in

their surrounding neural elements. Plasticity can affect the structure and

function of entire neurocircuits and entire systems comprised of multiple

neurocircuits operating in series and in parallel.

Imagine the accrued impact of synaptic plasticity and cellular plasticity

throughout an entire neural system. The change can be profound.

That change can ultimately be reflected in the organization of functional

representations we have in the brain. Consider, for example, the map of the

body that we have in our somatic sensory cortex.

That map is constantly being updated as we change the use of our body, or

perhaps, as the body becomes injured. So, plasticity is a means by which we can

constantly update and refresh the learning and the representation that we

store, even across an entire cortical area.

Well with such change pervasive throughout our organization of neural

systems and neural circuits, it's not surprising then that plasticity should be

the bases of basically everything we do in our nervous system that is predicated

upon learning and change. So, plasticity is the basis of memory,

it's the basis of acquiring the motor skill that you may have acquired in life,

be it in athletics or perhaps performance arts.

Maybe it's in a musical instrument whatever it may be involving the

acquisition of motor skill, there's been some plastic change at multiple places in

your nervous system that has made that skill possible.

The same would apply to cognitive skills. any domain of learning requires that

there be some plasticity. Certainly the development of language or

the acquisition of new languages throughout life.

mathematics for example, the ability to acquire new skills and then apply that

knowledge in problem solving. That's another example of plasticity in

action, as would be any of the dimensions of the performing arts as I mentioned a

moment ago. And finally, again, putting it back into

the context of healthcare, adaptation, and recovery from injury or disability

requires plasticity within the central nervous system.

So, let's just review some of the basic cellular mechanism of plasticity that

seem to apply to multiple forms of plasticity.

And we'll see how these are played out in different contexts.

So, plasticity usually begins when neural activity triggers the activation of

postsynaptic second messenger systems. And those second messenger systems

usually involve an alteration in the level of intracellular calcium in the

postsynaptic neuron. So calcium will be a key index that is

used by the postsynaptic neuron to know which way to go with its plastic

response. So calcium within the postsynapitc neuron

triggers the activity of second messenger systems that often converge on one of two

categories of enzymes. one category is the protein kinase family

of enzymes these are enzymes, that phosphorylate target proteins.

And that's often a mean of turning on that target protein.

Another category is phosphatases, and phosphatases are enzymes that

dephosphorylate target proteins. So, it's this alteration in protein

phosphorylation that mediates the early stages of synaptic plasticity.

Where new proteins don't need to be produced, so, so we've not yet really

altered the overall protein complement of the post-synaptic cell.

We've just altered the function of the proteins that already exist.

However, for the long haul, there must be long lasting change in synaptic strength

that's brought about by other mechanisms, those mechanisms that involve a change in

gene transcription. Well, all of these steps are common to

multiple forms of plasticity, and one key differentiator of one form or another is

going to be The level of calcium that's present in the post synaptic cell.

So, pay attention to where the level of calcium becomes critical for determining

what type of plasticity is observed. Okay so now we're ready to talk about one

particular mechanism of plasticity called long-term potentiation.

But before we can, I need to introduce you to a model system that was

foundational for the studies that first brought to light these mechanisms.

And that model system is the slice through the hippy campus from a rodent

Used as an animal model. So, these experiments can be done,

because when an animal is humanely sacrificed and its brain rapidly removed,

tissue slices can be obtained from that brain and those slices can actually be

kept alive for some period of time. perhaps as long as a day.

And during that time, those slices can be probed with microelectrodes, and axons

can be stimulated, and the activities of cells can be recorded.

And this is what was done from slices obtained from the hippocampus of rodent

models, so the hippocampus in the rodent is in the posterior part of the

forebrain. And is something of a C-shaped structure

with part of in the dorsal aspect of the forebrain, and the rest of it wrapped

around the medial margin of the lateral ventrical as it extends in the posterior

part of the forebrain. Now in primates, of course, the

hippcocampus has rotated further down into an inferior and forward position.

So, in primates, the hippocampus would be found in a position of the medial

temporal lobe. but of course, rodents don't exactly have

a temporal lobe. They have corresponding cortical regions

but not a lobular shape per se. Well, be that as it may, it's possible to

obtain sections through this hippocampus and keeps those sections alive in a dish,

if you will, and manipulate the activity of those cells while recording different

populations. This is all done with microelectrodes.

So, there's a particular circuit that you should be introduced to in order to make

sense of the experiments that I'd like to tell you about and it involves basically

a three neuron pathway through the hippocampus.

And it begins with inputs that arrive into a part of the hippocampus called the

dentate gyrus. And these inputs are coming from the

cortex just outside the hippocampus. And something called the entorhinal

cortex, part of the parahippocampal gyrus, which you may recall from viewing

the surface of the human brain from below.

And, these inputs make synaptic connections on a type of cell called the

granule cell. The granule cell then sends synaptic

inputs to a large pyramidal cell that's found in a region called the CA3 region

of the hippocampus. this large pyramidal cell sends axons to

several different places. One of them is to a different sector of

the hippocampus called the CA1 region. And it's this pathway from CA3 to CA1

that we're going to focus in on and use as our model system.

this axon that goes from CA3 to CA1 is called the Schaffer Collateral Axon.

And it's possible then to put micro electrodes into this system And stimulate

some number of these axons that might be converging on a pyramidal cell in the CA1

region. And the experiments that I'd like tell

you about are as follows. A particular microelectrode that is

positioned along this pathway is going to be stimulated.

So, over time, there may be a brief barrage of electrical pulses applied.

This may last just a couple of seconds at a very high frequency and this is called

a tetanus. So this kind of tetanic simulation is

what will be used to stimulate a pathway and induce long-term potentiation.

Meanwhile, a second microelectrode can be positioned to activate a different set of

axons that is present and functional, but just not stimulated with a tetanus.

Now, to measure the impact of the tetanus in the pathway that's stimulated, as well

as the parallel pathway that wasn't tetanized.

It's possible just to provide a test shock, maybe about once every 30 seconds.

And then, record from this post synapticcell, the amplitude of the

excitatory postsynaptic potential, and see what happens to that postsynaptic

potential. Does it stay the same?

maybe it increases. While this is the base, basic experiment

that was performed and the results are shown here.

So, Pathway 1 is the pathway that received that tetanic stimulation.

So, before the tetanus, a single electrical shock gave rise to a

particular excitatory postsynaptic potential of a particular amplitude and a

particular bit of rise. But then, after this tetanus, look at

what happened. The excitatory postsynaptic potential in

the same pathway, in response to a single shock, is about doubled in amplitude.

So this is long-term potentiation. Difference in the amplitude of the

response of that synapse to the test shock between the prestimulus condition

and the poststimulus condition. Something about that brief, tetanic

stimulation caused some fundamental change in the strength of this synapse.

So, now, it has twice the impact on the postsynaptic cell than it did previously.

Now, that was for the pathway that was stimulated with the tetanus.

Look at the parallel pathway that was not tetanized.

It's present, it's active. In response to a single shock stimulus,

it gives rise to a excitatory postsynaptic potential just like the

neighboring pathways, only now, before and after the application of the tetanus

to Pathway 1, there's no change to Pathway 2.

No change, no LTP. Here's another way to look at these data.

Plotted here are the responses in these two pathways to the single test shock

applied about every 30 seconds or so, for about 15 minutes, before the tetanus to

about an hour afterwards. And what we see in Pathway 1 is about a

two to threefold increase in the amplitude of the EPSP over time.

Now, there is some decay of this potentiation over the course of this

experiment lasting about an hour. But nevertheless, after about one hour of

time, there is still about a twofold increase in the amplitude of that EPSP,

the excitatory postsynaptic potential in the pathway that was tetanized.

In the pathway that was not tetanized, there's essentially no change.

Now, these initial experiments were done at a time when slices in a dish could be

kept alive for about a day or so. but what one really wanted to know was

whether this potentiation might be a mechanism of learning and memory over a

much longer period of time and that required in vivo experiments.

And indeed, this has been done, and we now have a compelling body of data

suggesting that long-term potentiation may indeed be the mechanism by which

information is stored across a lifetime. Well, this is not a lifetime, but for

Rodin, it's still a very long period of time within his lifespan.

Notice, that following the application Of o tetanic stimulation, there is a

significant increase, in the amplitude of the excitatory postsynaptic potential

recorded in vivo, out for about a year's time.

So now we're beginning to gain confidence that long term potentiation may be one

means of storing information at the synaptic level across a lifetime.

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