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Neuro: 2:00 - 3:00
Scribe: Caitlin Cox
Wednesday, March 11, 2009
Proof: Marjorie Hannon
Dr. Wyss
Learning and Memory
Page 1 of 7
*He tells a lot of stories and I did type them all out so that you can really understand the points he is making, but I
asked him and you do NOT need to know any details of the stories. Just know the main points he is making
through them. He said test questions will be based on what is on the last slide.
I.
Learning and memory as an integrative process [S1]:
a. At the end of the lecture, there are a bunch of questions that you should know for the test.
II. Numbers Chart [S2]:
a. You have 30 seconds to memorize this chart. He will test you on it at the end of the lecture.
III. Definitions [S3]:
a. Learning is an adaptive change in behavior brought about by experience and involving a CNS neuronal
mechanism.
b. Plasticity occurs all over. There is memory in the immune system, in muscle, etc.
c. But learning is specific to the CNS, so it has to be in the brain or spinal cord.
d. Memory is storage and recall of a past experience and that’s important because that is what you have to dreg
up to take tests, for example. It is what you have to do in order to remember how to fix an impacted tooth or
what you need to do to refract an eye. You need to be able to recall that into memory.
IV. Terminology of Learning [S4]:
a. There are different types of memory. Two major characteristics are:
i. Declarative memory, which is accessible to conscious recollection, so you can talk about it.
ii. Procedural memory, which are skills and habits. But they are skills and habits that you don’t have verbal
access to. Once you become proficient and your mentor says he/she has finally got hands, you cannot
really explain what you are doing on that tooth or on that refraction, you just do it, it is automatic.
iii. What does that tell you about procedural memory? Is it absolutely separate from declarative memory?
Probably not. Those of you who play the piano well, when you first learned to play, did you have to think
through where every key was located? You had to think through the scale, but if you had to still do that,
you would be a terrible pianist. Initially, some things have a declarative aspect to them where you can
verbalize what you are doing, but in order for that to become efficient, you need to move it on to procedural
memory. We will see that procedural memory is consolidated in a very different location.
V. Memory Diagram [S5]:
a. First, we’ll talk about procedural or “implicit” memory.
b. On the diagram, you can see that skills, habit, emotional associations, and conditioned reflexes all use this
group of regions in the brain for their processes: the striatum, motor areas of cortex, cerebellum, and amygdala.
c. That is quite different from declarative (or “explicit”) memory which uses the hippocampus and the neocortex.
VI. Classical Conditioning [S6]:
a. Example is procedural memory. You repeat stimuli together and they become associated.
VII. Figure 55.2 [S7]:
a. You all know the Pavlov dog study: he would ring a bell (the dog could not care less about the bell), but then he
would ring the bell and present a hamburger right after. If he repeated those two together consecutively enough
times, then eventually when he rang the bell, even though the hamburger was not there, the dog would salivate
as if the hamburger were there. He had fixed that association.
b.
c. A.R. Thompson, an innocuous tone. Eventually the rabbit will learn when it hears the tone to blink its eye.
d. Cerebellar cortex that
VIII. Figure 55.12 [S8]
a. The areas of the brain that that uses is shown here by a different experiment by Thompson.
b. In this experiment, he played an innocuous tone, so you are conditioning to that tone. Then he had an air puff
onto the cornea of these rabbits. He asked where are the areas subserving the memory because eventually the
rabbit will learn that when it hears the tone to blink its eye.
c. What he found is that areas you would not think were associated with memory actually were. These were areas
in the cerebellum, the deep cerebellar nuclei, the interpositus nuclei, and the cerebellar cortex that subserves
those deep nuclei. So the information came in, it routered up to the cerebellum, and then it was consolidated
here and the learn trait took place there.
d. The important things to remember about procedural memory are that they are habits, they are things you cannot
verbalize, and that the memory consolidation for these occurs in the cerebellum. It seems to be a parallel
pathway to declarative memory.
IX. Declarative (explicit) Memory [S9]:
a. Declarative memory is accessible to consciousness and you can verbalize it.
X. Capacity for Declarative Memory Storage [S10]:
Neuro: 2:00 - 3:00
Scribe: Caitlin Cox
Wednesday, March 11, 2009
Proof: Marjorie Hannon
Dr. Wyss
Learning and Memory
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a. Capacity for declarative storage is enormous. Even though you think as you study for a test that you only have
so much room in the brain as you binge and purge information, it is not true.
b. A college student got bored and started spending 1 hr/day practicing remembering numbers. Each day he
added a few more. In the end, someone could read him numbers at the rate of 1 per second and he could
repeat up to 90 of those numbers that were given to him in a single sitting. He is very rapidly able to gain this.
c. You guys can do about 9; the length of a telephone number; that’s about your normal capacity.
XI. Capacity for Storage [S11]:
i. A couple more examples to show that you have a less limited declarative memory than you might think:
ii. Toscanini was a great composer and director. One day he was getting ready to lead Beethoven’s 5th and
the bassoon player came up to tell him he could not play because he had broken his B flat. Toscanini
thought for a second and then said there is not a B flat in today’s symphony for the bassoon so no problem.
He knew about 200 scores like that.
iii. Alexander Aitkin could recite the power of π to 1500 digits at age 16. What is amazing is that at 30 years
of age, the computers estimated what π was and he found there was an incorrect digit at digit number 840.
He corrected that and learned it up to 2500. That is really nothing now because the Japanese winner of
the latest competition is doing around 97,000 digits.
XII. Strategies [S12]:
a. What strategies do you use for memorizing information?
i. You might repeat it a lot.
ii. Do drugs not war. Viagra works reasonably well for remembering. It does seem to work; it also cures jetlag according to literature.
iii. Images are often used. If you can’t remember something, you have an image of that and you know it is
there, you can see it in the book, you can image it, then all of a sudden it becomes clear and you can
answer the question.
iv. Relationships. All of you know the dirty limericks for gross anatomy. If you can put it to song, you can
remember the tune and then eventually remember the embedded information within that song.
XIII. Human Declarative Memory [S13]:
a. What’s the underlying network of information flow? There are two processes:
i. First one has to encode the memory, and then you have to have the ability to retrieve the memory.
1. During the encoding process of memory, memory easily disrupted.
2. The common wisdom is that once information is consolidated and sent off to its final destination for
storage, that that recall does not appear to be disturbed very often.
3. The question becomes, though, is that information is malleable. (This will be discussed later in the
lecture.)
XIV.
Loss of Memory (Amnesia) [S14]
a. It is the loss of memory patients that have really informed us initially about the pathways being subserved by the
memory system.
b. The first of these came from a neurosurgical screw up, so doing the right thing, but still screwing up badly.
c. We will see one patient’s trauma, another’s ischemic damage, and finally Alzheimer’s as far as the pathways
ECS.
XV.
Neurosurgery [S15]:
a. Patient HM fell off of his bike and hit his head. From that time at 9 years old onward, he had Gran Mal seizures
often. The seizures were intractable to any medication that was available at the time. A neurosurgeon noticed
that the seizures started in the right temporal lobe and spread to the left temporal lobe, and decided to blow out
the temporal lobes to cure his epilepsy because the temporal lobes were thought to be connected to the
olfactory system, which would not necessarily have been a problem to lose. He retracted the hippocampal
formation and associated cortices on both sides, knocked out the entire temporal lobe. Unfortunately, that left
the patient profoundly amnesic with normal short term memory, a little bit of intermediate memory, and no ability
to encode new memory.
b. What is important to note is that although he had no ability to encode new declarative memory, he had very
good ability to recall anything that occurred prior to the surgery. He had almost perfect recall, better than normal
recall of information.
c. The second point to note about this patient was that his procedural memory was perfectly intact. He was an
engineer, and he did a lot of drafting. If you asked him to do a drafting task, he had no problem doing it, no
problem learning a new drafting task. But he had no idea that he did it or how he did it. So he had procedural
memory abilities but no declarative memory abilities.
XVI.
HM studied by Brenda Milner and others [S16]:
a. Brenda Milner, a psychology student, followed Patient HM up until his death. She noted that when he came into
her office, she would ask for his wallet, and he would give it to her. She would place it on the file cabinet behind
Neuro: 2:00 - 3:00
Scribe: Caitlin Cox
Wednesday, March 11, 2009
Proof: Marjorie Hannon
Dr. Wyss
Learning and Memory
Page 3 of 7
her and say “It’s right here” and he would say “Okay.” She would ask him where it was, and he would say right
there. 2 seconds later, she would ask him where it was, and he would say right there. Then she would talk to
him about how he got there and what he ate. 20 seconds later, she would ask “Where is your wallet?” and he
would look for it and say he must have forgotten it.
b. He also moved after his surgery but kept going back to his old home without any recollection that he shouldn’t
be there.
c. He had good long term memory from past events, no ability though to bring new information forward.
d. That focused attention on the hippocampal formation as involved in memory.
XVII. Focus on the hippocampal formation as site of short- to long-term memory encoding [S17]:
a. Until this time, everyone had looked for where the memory is stored. Now the search went for where is the
memory process taking place.
b. The hippocampus was first looked at.
c. At the time this was considered to be an olfactory brain that didn’t have to do with anything and that we had all
these useless parts of the brain that were just hanging out. However, that is not the case.
XVIII. Drives, Emotions, and Memories: The Hypothalamus and Limbic System [S18]:
a. Here is the hippocampal formation in a mid-sagittal view. The hippocampal formation is lying down in the
temporal lobe and running on up toward the cingulate cortex.
b. Cingulate cortex is involved in spatial memory. (This will be discussed later but he mentioned it here.)
XIX.
Lateralization [S19]:
a. Patient NA was a 20 year old air force man. His roommate stabbed him by accident with a fencing sword. It
went through the right nostril and up into the left temporal lobe.
XX.
NA and the Model Airplane Disaster [S20]:
a. The patient had severe anterograde amnesia for declarative memory.
b. In 1986, an MRI demonstrated severe medial temporal damage.
c. Good IQ (124) and language skills.
d. What is important about this patient is that mostly verbal amnesia with little appreciation for current events,
forgets story lines during TV commercials but excellent at drawing from memory.
e. What is interesting about this patient, though, is that he was not able to remember event very well, but he was
able to remember new verbal information a little bit better, and he could figure out new strategies to use
language. So he could do crossword puzzles fairly well, and so forth.
f. What would that tell you about him? It is left side temporal lobe damage, so that means you have this
somewhat damaged verbal, it means that there must have been some change in where verbalization is taking
place.
g. The verbal skills were lost; the nonverbal skills were not lost. Does that tell you anything?
h. When presented with graphic information, he is able to remember it, but verbal skills he lost.
i. Where is verbal skill located for most people? Left lobe.
j. By NA losing his verbal skills that suggested that memory consolidation for verbal skills takes place in the left
hippocampus. Whereas, other declarative-type information that is non-verbal takes place in the right
hippocampal formation.
XXI.
Hippocampus [S21]:
a. Patient RB was a mail carrier in San Diego. He went in for surgery. The surgery was uneventful, but then later
he had a sudden atrial tear and loss about 5 liters of blood. He seemed normal the next day, but he had lost the
ability to encode long-term memory.
b. He did not have quite as intense a deficit as HM did, but it was still a huge deficit.
c. His procedural memory seemed to be intact, but he did not have the ability to encode declarative memory.
d. Patient died and during the autopsy they found that there was only a single area of the brain that showed a
disturbance.
XXII. RB [S22]:
a. That area was CA1 of the hippocampal formation. This is the small pyramidal cell layer in the hippocampus.
b. In general, we think about the hippocampus as serially processing information: it comes in one portion and
goes out through pyramidal cells and finally the CA1 pyramidal cells send it on back out into the neocortex.
c. Patient RB has had that circuit broken at one selective point. They sectioned his entire brain and the only
damaged part was that the CA1 cells were gone. CA1 cells happen to be extremely sensitive to ischemia,
which is why they died in this case.
d. It is a very selective loss; it is a loss often seen in MI patients, at least partial loss. Again, probably dependent
on the fact that it is a single area of the hippocampal formation that is lost.
XXIII. Figure 5 Diagrams [S23]:
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Proof: Marjorie Hannon
Dr. Wyss
Learning and Memory
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a. RB is the solid line. This is him being seen in different public events. He seems to be as good as or better than
normal control patients. However, in encoded long term memory of events after the surgery, he has very little
ability to encode that memory.
XXIV. Figure 55.19 [S24]:
a. This just shows you an example of the hippocampal fields have a dentate gyrus (you don’t need to know this).
These are the pyramidal cells. The information flow normally is thought to occur coming from neocortical and
entorhinal regions into the dentate gyrus granule cell from there into the CA1 large pyramidal cells, from there
axons carrying it to the CA1 cells, from CA1 cells back out to the cortex. You do NOT need to know the circuit,
just know there is serial processing.
b. What happens when this area is knocked out? It appears that the serial processing can no longer take place,
and thus, the brain can no longer easily encode new memories.
XXV. Apparent lessons from the patients [S25]:
a. Hippocampus important for declarative but not procedural memory.
b. Hippocampus important for converting short- to long-term memory.
c. CA1 is critical to declarative memory.
d. Temporal lobe has function in emotional memory.
e. Memory may be lateralized.
XXVI. Figure 56.4 [S26]:
a. Here is the pathway for the memory circuit.
b. A large area of the cortex, especially sensory areas of the cortex sending information into the cortex around the
hippocampal formation, including the entorhinal cortex.
c. Serially processing it through the hippocampus and subicular areas and then coming back out to cerebral cortex
from there.
d. It is only a temporary processing station for the brain
e. In general, it keeps information in that process for somewhere around 24 hours to perhaps 2 days.
f. You just had a lecture on circadian rhythm. It is in the sleep cycle that the circuit opens up to allow information
in the hippocampal formation to easily pass out into the neocortex to gain registry for permanent memory.
During other states of the wake cycle, this system is fairly closed, so permanent memory is not laid down, it is
thought, in most individuals until this circuit is opened by nor adrenaline during the sleep cycle.
XXVII. Animal studies have helped to clarify the memory circuits [S27]: (He just read the title of this slide.)
XXVIII. Figure 59.1 [S28]:
a. This is just showing an example of the test the primate was given.
b. First, if you show the monkeys a bus, then show them a bus and a piece of cake. If the task asks him to pick
out what he just saw, the monkey does not have a problem doing that. Even damaged monkeys will pick out the
bus, but if you ask him to delay from seeing this and then ask the monkey to pick out what he did not see, it
becomes a much more difficult task.
c. This case is called the delayed non-matching example.
XXIX. Hippocampal damage does not alter motor skill [S29]:
a. For an animal with hippocampal damage, motor skills are perfectly intact, short term memory is perfectly intact,
procedural memory is perfectly intact.
XXX. Large Hippocampal lesions disturb declarative learning [S30]:
a. But now you ask him to do this delayed non-matching example and as the delay gets longer between what they
saw and when they are asked, animals with large hippocampal damage show a significant deficit in their ability
to carry out this task.
b. When looking at information like this, you have to consider how long the delay is and how hard the task is. A lot
of literature out there uses very simple tasks and tells you that the individuals they looked at had no deficit.
Typically, they’ll use the Mini Mental Status Examination (MMSE). That is a great examination if you are trying
to differentiate an Alzheimer’s patient from you. But if I gave all of you that examination, I couldn’t differentiate
anything even though there are probably different learning abilities within here. Or if I were to look at you versus
a normal aging individual, although their memory consolidation is different than yours, I’m not going to see any
difference with that test.
c. The delayed non-matching example test worked in this case.
XXXI. Hippocampal formation affects learning not retention [S31]:
a. This just shows that the memory consolidation takes place over a few days but not months.
b. In this case, if one teaches the animal a non-matching example task, lesions the hippocampal formation the next
day, that animal cannot perform the task it just learned.
c. However, if you train the animal up to criteria, then you lesion the animal a month later, the animal remembers
the task perfectly well.
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Proof: Marjorie Hannon
Dr. Wyss
Learning and Memory
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d. That just tells you that the hippocampus is processing the information but it is only a short term processor,
eventually the memory storage takes place somewhere else.
e. This agrees with the human patient stories discussed previously.
XXXII. Other limbic areas involved in learning and memory [S32]:
a. Other limbic areas involved in learning and memory includes: the perirhinal cortex, the cingulate cortex and the
amygdala. All three of these have a unique processing component.
b. Perirhinal cortex does have some ability to show memory even when the hippocampus is lost.
c. Cingulate cortex is primarily spatial memory
XXXIII. Mammillary bodies of hypothalamus and medial thalamus [S33]:
a. Korsakoff’s syndrome:
i. Caused by Vitamin B1 deficiency, which is secondary to malnutrition in alcoholics.
ii. Correlated with a loss of mammillary bodies.
iii. The subiculum of the hippocampal formation has a huge projection there. But they were wrong. If you
knock out the mammillary bodies in primates, it does not do anything. It looks like there is secondary
damage in the mediodorsal thalamus. That is the damage that is really important in this case.
iv. The damage ends up being not so much related to the memory circuit as being related to the prefrontal
cortex. Prefrontal cortex does executive function, motivation, and superego.
v. These patients don’t have a memory problem; they have a problem doing anything—they have an
executive problem. You’ll see them in your office; you will ask them a question and they’ll give you an
answer that sounds true but when you talk to their caretaker you will find out that they made it all up. They
sound logical, but the prefrontal cortex is gone.
XXXIV. Cingulate Cortex Diagram [S35]:
a. In the midline, cingulate cortex has two areas involved. One of those is involved in spatial memory; it allows you
to navigate in space. The other (the more frontal regions of the anterior cingulate) is involved in the autonomic
responses to learning because if you are going to learn something you have to have sympathetic nervous
system turning on to some extent locations. You have to have noradrenergic system in the brain appropriately
turning on and off in certain areas so that that memory is consolidated. Stress hormones have to be up;
depending on where they are, you are either going to remember or not remember an event that occurs.
XXXV. Figure 6 [S36]:
a. Lesions of the amygdala.
b. The amygdala is primarily processing emotional information. This is in the procedural side. If you knock out
hippocampus, as shown in this diagram, you knock out the memory circuit. You don’t do anything to emotional
learning.
c. In contrast, if you knock out the amygdala, you knock out the emotional response, the emotional memory is
gone, but the normal declarative memory is intact.
XXXVI. Figure 56.12 [S37]:
a. This just shows you the connections of the amygdala. It is tied into the hormonal system; it receives input from
the hormonal system and sending it back. (You do NOT need to learn the circuit.) Recognize that the
amygdala gets a large number of inputs and that it sends that input out to the cortex as well as back to other
learning memory portions of the circuit for procedural memory encoding.
XXXVII. Lateralization of the memory circuit [S38]:
a. An important point is that the amygdala is lateralized for its memory components. In this study shown, rats were
in a step-through box and were placed in the light side of the box. Rats are nocturnal; they want to go to the
dark side of the box. But if they jump into the dark, they get shocked. The idea is that a smart rat will stay on
the light side as long as it can until it cannot stand it any longer, then it will jump into the dark side and get
shocked.
XXXVIII.
Figure 2 [S39]:
a. This shows that if you bilaterally lesion the amygdala using lidocaine, the animal cannot withhold the response
to jump to the dark side.
b. If you only lesion the left amygdala, you do not get this affect. They look like the control animals. But if you
knock out the right amygdala, you again get no ability of the animal to withhold their response, so they jump
through and get shocked immediately.
c. This tells you that there is lateralization even in these deep areas of the brain.
d. Most people don’t recognize that these deeper areas have similar lateralization.
e. There’s also clear lateralization even in the control of heart rate. The left amygdala has more control over heart
rate than the right amygdala. When you get ischemic damage to the left amygdala, you get arrhythmias in the
heart and sudden death. You never get that with right amygdala lesions. (This stuff will NOT be on the test!)
f. Even in these autonomic areas, there is lateralization and certainly lateralization in the memory circuit.
XXXIX. Aversion memory demonstrates other mechanisms involved in different types of memory [S40]:
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Dr. Wyss
Learning and Memory
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a. All of you have had this; in this case it is a one trial event.
b. Who has been to a restaurant and gotten sick that night? How soon did you go back to that restaurant? You
did not want to go back there. This is one trial learning.
XL. Garcia and Koellinger [S41]:
a. Rats were given taste stimulus and then irradiated so that they got sick. The taste stimulus did not do anything.
b. After recovery, the rats refuse to drink that taste stimulus; they would starve to death before they would drink it.
c. The taste most effective was lithium chloride.
d. Differences from associated learning:
i. Only 1 trial was needed.
ii. Delay between CS+ and US can be hours. Normally, CS+ and US have to be within seconds of each
other.
e. The reviewers of the best journal of neurology said that this study was as ridiculous as “the bird defecating in a
cuckoo clock.”
So if you ever get a bad review, don’t worry about it because they clearly knew what they
were doing.
f. That is one trial learning; that is learning in which you are presented with a very noxious stimulus and for a long
time you will not return to the stimuli surrounding that time. The restaurant had nothing to do with the fact that
you got the flu that night, but you won’t return to that restaurant for a long time. It is long term memory, it is
protective and adaptive. It makes sense because you don’t want to do anything that might endanger your being.
XLI.
Aging [S42]:
a. Normal aging associated with slow shrinkage of the brain due to loss of synapses in neuropil.
b. Dementia shows exaggerated shrinkage due to loss of neurons and synapses in neuropil.
XLII.
Age vs. Brain Weight Graph [S43]:
a. The bad news is that all of you are over the hill; you peak at age 18. But luckily it is a fairly slow downhill in
normally aging individuals.
b. The average brain size changes with age.
c. Clearly, whereas most individuals show this shrinkage and there is some loss in the ability to encode memory,
that is very minor and it follows the same very slow progression through about 80 years of age.
XLIII. Alzheimer’s Disease [S44]:
a. In individuals with Alzheimer’s disease, the gradual loss in memory accelerates greatly and it is associated with
the loss of cognitive and emotional function.
b. It is not an isolated event because the plaques and tangles in the neuropil. This disturbance and loss of neurons
is not only in memory circuits, it is also in other portions of the brain circuit processing other information.
c. Loss of acetylcholine from basal forebrain. Acetylcholine potentiates memory circuit and its loss leads to a
decline in that.
d. There is poor correlation with damage of functional deficit and areas like the medial geniculate are also affected,
so it is not just a selective loss of memory. But certainly in these patients, there is a great loss in learning and
memory.
e. You will have a fair number of patients who have this disease.
XLIV.
[S45-46]: Skipped because they are repeats of Slides 40-41.
XLV.
Is memory unwavering? [S47]:
a. The idea we have built up at this point is that you process the information at the hippocampus, it goes out to the
cortex, it sits there and for as long as you live, you can recall that information.
b. William Penfield did a lot of studies stimulating the brain. He found that there were areas that he could stimulate
and the person would suddenly recall experiences when they were 5 or 6 years old. He verified those
experiences with the parents. Otherwise, they were unable to recall that detail.
c. That all led to the idea that you have this non-malleable information storage that you may not be able to access,
but if you can access it, then you can access this perfect memory storage.
XLVI. Patient S (Shereshevskii) [S48]:
a. AR Luria’s patient who was a reporter for the Moscow Times. One of his assignments was to go and listen to
the czar’s speech which usually was about two hours in length. He did not take notes but was able to rewrite
the czar’s speech perfectly word for word.
b. Patient S had no apparent limit to memory, everything you showed him, he memorized.
c. He had no apparent short-term memory; everything went straight into long term memory.
d. He had no ability to forget.
e. He had a miserable life because he could never forget anything.
f. It seemed to break this idea that everything had to go to the hippocampus first.
XLVII. Number Chart (again) [S49]:
a. What was third row over, seventh number down? --0
b. Patient S had about 200 of these memorized.
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Dr. Wyss
Learning and Memory
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c. Importantly with S we see some ability to store information immediately.
XLVIII. Forgetting [S50]:
a. Forgetting occurs early in the memory process.
b. Not all that is learned is remembered and we readily forget what is unimportant. You have this information in
short term memory but you don’t need it for long term. You need it in order to navigate a particular procedure,
but you don’t need it in the long term, so you forget it.
c. For events that we initially memorize, we forget some of those or are unable to recall them.
XLIX. Average rate of forgetting for declarative events [S51]: Skipped
L. Forgetting model [S52]: Skipped
LI. Forgetting is an active process [S53]:
a. It is driven by NMDA.
b. Other information coming in the circuit will wipe out the ability for past information to be consolidated.
c. Every piece of information that’s circulating in the hippocampus has to be weighted for its importance. And
according to that importance, either it will eventually run out into long term memory or it will be lost.
d. Unimportant information is easily forgotten when other information comes into the system.
e. So an active process of forgetting; getting rid of information that is not necessary; you don’t remember every
single detail that you have ever experienced.
LII. Nadel hypothesis that hippocampus remains active throughout many memories lifetimes [S54]:
a. Nadel looked at MRIs to see if the hippocampus plays any role when you recall memory.
LIII. Figure 6: Schematic renderings of remote and recent activations [S55]:
a. What he found was that hippocampus lights up when remote events are recalled and when recent events are
recalled. And it’s the same areas that light up.
b. His idea was that perhaps the hippocampus is involved in recall memory.
c. It may be that if you don’t have a hippocampus you can still recall that information, but maybe it is involved
during recall. That fits in very nicely to the last set of information I want to give you about if information during
recall becomes malleable.
LIV.
Does information during recall become malleable? [S56]:
a. Idea that you can change a witness’s testimony, a witness’s recall of information. They actually recall it, you
give them other information, and that new information feeds into the old information.
b. There are human and animal studies that suggest the possibility that especially in emotional/stressed events,
when recalled can go back into the hippocampus and information/input occurring at that time of recall can fit into
the old memory. So when it is sent back out for storage, it is the old and the new mixed together.
c. It is not clear how often that occurs.
LV. [S57-62]: Skipped
LVI.
Summary of Important Concepts [S55]:
a. Declarative vs. Procedural memory: Know the differences and the circuits underlying each, especially
hippocampus, neocortex, cerebellum, striatum, and amygdala.
b. Role of hippocampus is a “temporary” processing station and perhaps as a playback station.
c. Role of amygdala in emotional memory
d. Age-related changes in learning and memory. Normal changes being very slow but very much accelerated in
diseases like Alzheimer’s or Parkinson’s.
e. Forgetting and potentially alteration is, in part, an active process that can continually occur.
[end 50:20 min]