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Psych 314 > Chapter 12 The Biology of Learning and Memory > Flashcards

Chapter 12 The Biology of Learning and Memory Flashcards

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1
Q

Localized Representations of Memory [placeholder]

A

.

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2
Q

Pavlov’s classical conditioning

A
  • unconditioned stimulus (meat) automatically elicits an unconditioned response (dog salivates)
  • conditioned stimulus (tone) initially elicits no response
  • conditioned response (dog salivates to tone) is learned with repeated pairings of tone with meat
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3
Q

Localized Representations of Memory cont. [placeholder]

A

.

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4
Q

Operant Conditioning

A
  • an individual’s response is followed by a reinforcement or punishment
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5
Q

Reinforcement

A

is an event that increases the future probability of the response

—> e.g.: given fruit loops for a correct response, a rat learns to return to the same arm of maze

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6
Q

Punishment

A
  • is an event that suppresses the frequency of the response

—> e.g.: given a shock for the wrong response, a rat learns to avoid arm of maze

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7
Q

Engram

A
  • the physical representation of what has been learned (e.g., a connection between two brain areas)
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8
Q

Karl Lashley searched for the ….

A

Engram

  • he trained rats on mazes and brightness discrimination tasks (memory tasks) and made cuts between two brain areas or removed part of the brain

—> none of the deep cuts disrupted maze performance

—> maze performance was only decreased when very large amounts of brain were removed (not small areas)

  • So learning and memory does not depend on a single cortical connection or area
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9
Q

So from this, Lashley proposed two principles

A
  • equipotentiality
  • mass action
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10
Q

equipotentiality

A
  • all parts of the cortex contribute equally to complex behaviors like learning
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11
Q

mass action

A
  • the cortex works as a whole, and the more cortex the better [main difference between this and equipotentiality]
  • incorrectly assumed that all kinds of memory were physiologically the same and that the cortical area was the best place to search for an engram
  • But pretty good for being the first! (he did this in the 1950s)
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12
Q

lateral interpositus nucleus (LIP) of cerebellum

A
  • critical for classical conditioning of the eye-blink response
  • plays a crucial role in motor learning and coordination.
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13
Q

Modern Search for the Engram [placeholder] {info dump}

A
  • 1986 - Thompson et al: in a classical conditioning task, they paired tone with puff of air in eye until rabbit blinked at tone

—> found changes in cells in the lateral interpositus nucleus (LIP) of cerebellum

—> when LIP was cooled or drugged the rabbit did not learn and later when effects wore off rabbit learned at same rate as new rabbits

  • Conclusion: LIP has to be active to learn
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14
Q

Red Nucleus

A

(mid-brain motor area that receives input from LIP)

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15
Q

Modern Search for the Engram cont. [placeholder]

A
  • Thompson et al then suppressed activity in red nucleus (mid-brain motor area that receives input from LIP)

—> rabbits showed no response during training

—> when effects wore off rabbits showed strong learned response to CS

—> thus, red nucleus necessary for performance, not learning, of response

—> And the LIP really strongly looks like it’s involved in learning! (at least in rabbits)

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16
Q

Modern Search for the Engram cont. even more

A
  • Probably same in humans

—> classical conditioning of eye blink produced activity in cerebellum, red nucleus and other areas

—> people with damage to cerebellum are impaired at eye-blink task

—> But people with cerebellum damage aren’t impaired in other types of learning tasks.

  • So, just like with vision, learning in humans is most likely done in several different locations, depending on what type of memory is needed.
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17
Q

Hebb: Short and Long-Term Memory [place holder]

A

.

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18
Q

Short-term

A
  • events that have just occurred
  • limited capacity, around 7 unrelated items
  • Why phone numbers are 7 digits (seriously!)
  • If forgotten is lost forever – can only get it into LTM through rehearsal. Hints don’t help
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19
Q

Long-term

A
  • events from previous times
  • not lost, are recoverable, and hints help
  • HUGE capacity – never appears to get full – when you learn something new, you don’t have to forget something old to “make room for it”
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20
Q

Consolidation

A
  • is the process of converting short term memory to long term memory
  • memories that stay in short-term memory long enough are formed into long-term memory
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21
Q

Consolidation of Long-Term Memory [info dump]

A
  • To study consolidation, researchers used shocks to disrupt memory, looking for short-and long term memory threshold

—> but, shock to head disrupted both short-term and long-term memories

—> also, some disrupted memories could be recovered after reminder of event

  • Human studies weaken the distinction between short- and long term memory

—> we can recall events more than a few hours, or days, old but nevertheless will be forgotten in near future

—> So obviously, at least in humans, it’s not quite as simple as STM and LTM

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22
Q

Consolidation of Long-Term Memory cont. part 1 [info dump]

A
  • When we learn, the learning activates several genes that promote learning and memory. It also activates a gene that produces PP1
  • Protein phosphatase 1 (PP1) interferes with memory retention by inactivating genes that promote learning

—> This is actually adaptive – it allows us to easily forget single experiences, as we don’t need to remember every single thing that ever happened to you

—> PP1 accumulates during massed practice and declines during distributed practice (why cramming is worse for memory retention than spread out learning)

—> So if you really attend to what you’re trying to learn and learn it in an appropriately spaced manner, the learning genes will be stronger than the PP1 and you’ll remember it. If not, the PP1 “wins” and the memory is lost

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23
Q

Consolidation of Long-Term Memory cont part 2 [info dump]

A
  • Consolidation is gradual and we recall older memories more easily

—> It appears that the earlier a memory is, the more firmly it’s implanted in our memory

—> older people showed most MRI activity to celebrities in the 1990s and least to celebrities in the 1940s

—> people showed more temporal lobe activity to places visited in last 2 years than those visited in last 7 years

—> Interpretation is that we have to work harder to get the newer memories, but over time, they will get more firmly ingrained

  • Meaningful and emotional experiences enhance memory consolidation, e.g, receiving award or being in car wreck

—> Emotions increase secretion of cortisol and epinephrine

—> epinephrine stimulates vagus nerve which excites the amygdala; cortisol stimulates the hippocampus – big in memory!

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24
Q

Consolidation of Long-Term Memory cont. part 3

A
  • Direct injections of cortisol or epinephrine enhance storage and consolidation of memories

—> but prolonged stress results in too much cortisol and memory is impaired

  • After damage to amygdala, emotional arousal does not enhance memory storage

—> If I gave you a list of 30 words to memorize and some were emotionally charged (taboo), like bitch or penis, you’d remember those more than the non emotional words like boot or apple.

—> But patients with amygdala damage didn’t remember “taboo” words better

—> So the amygdala is involved in emotional memory storage

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25
Q

A Modified Theory: Working Memory

A
  • Needed a more complex alternative to just STM and LTM
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26
Q

Working memory

A
  • we actually store information in LTM by working with it or attending to it
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27
Q

3 components of working memory

A
  • visuospatial sketchpad
  • phonological loop
  • central executive
28
Q

visuospatial sketchpad

A
  • stores visual information
29
Q

phonological loop

A
  • stores auditory information independent of visual memory
30
Q

central executive

A
  • directs attention toward one stimulus or another
  • In other words, just like in vision, the nature of the incoming information determines how it affects the brain and we have different parts of the brain to deal with different types of info
  • Presumably there are other components for touch, smell, and taste, but we just haven’t found them yet
31
Q

Baddeley & Hitch: Working Memory cont [placeholder]

A

.

32
Q

Prefrontal cortex appears to store ….

A

Working memories

  • shows high activity during delayed response tasks performed by humans and other mammals

—> also in tasks requiring different responses to signals given only after a delay

  • the stronger the activation in this area the better the performance
33
Q

Hippocampus and Amnesia [placeholder]

A

.

34
Q

Amnesia

A
  • memory loss, most famous px = HM
  • H.M. had hippocampus removed which resulted in
  • IQ and language abilities intact
  • moderate retrograde amnesia for events 1-3 years before operation
  • Also had anterograde amnesia - could not remember events after the operation

—> could not learn to find way to bathroom in hospital

—> could not remember telling story a few minutes later

-could define common words but not infrequently used words; also never learned newly invented words like Jacuzzi and granola

  • can learn new facts slowly, e.g., floor plan of home over many years
35
Q

H.M. cont.

A

.

36
Q

declarative memory/explicit memory

A
  • the conscious intentional recollection of facts information or concepts
  • deficit: can’t state memory in words
  • deficit: can’t recall some memories in response to question, e.g., who are characters in novel?
37
Q

procedural memory/implicit memory

A
  • intact: can develop motor skills
  • muscle memory

—> can read words written backwards

—> can draw something seen in mirror

better: experience influences behavior even if not remembered, e.g., always chose person who was friendly to him

38
Q

Skip

A

deficit: can’t recall some memories in response to question, e.g., who are characters in novel?

  • the conscious intentional recollection of facts information or concepts
39
Q

Skip

A

better: experience influences behavior even if not remembered, e.g., always chose person who was friendly to him

40
Q

Summary of amnesia from hippocampus loss/damage

A
  • Normal short term and working memory
  • Severe anterograde amnesia for declarative memory (difficulty forming new declarative memories)
  • Moderate retrograde amnesia – loss of some memories from before the brain damage
  • Intact procedural memory
  • Better implicit than explicit memory
41
Q

Function of the Hippocampus [info dump]

A
  • It appears that once memories are consolidated, they are “housed” in the cortex, not hippocampus
  • So what exactly does hippocampus do? – Hard to answer!
  • Some support for critical role in forming new declarative and explicit memories
  • Some support that the hippocampus is especially important for spatial memories

—> Taxi drivers have larger hippocampi than non drivers, taxi drivers who’ve done it longer have larger than newer ones, and answering taxi route questions activated their hippocampi more than answering non-spatial questions

—> damage impairs performance on spatial memory tasks, e.g., finding your way from one place to another

—> rats with damage here often forget where platform is under murky water

42
Q

Korsakoff’s Syndrome (aka Wernicke-Korsakoff syndrome

A
  • Brain damage caused by long-term thiamine (B1) deficiency
  • Thiamine is needed by the brain to metabolize glucose (fuel)
  • Prolonged deficiency leads to shrinkage and death of neurons throughout brain

—> especially in hippocampus and thalamus axons to prefrontal cortex;

  • Most typically seen in chronic alcoholics (why?)
  • Leads to apathy, confusion, amnesia
  • better implicit than explicit memory
  • difficulty ordering past events
  • confabulates, i.e., remembers guesses as true memories (not purposefully lying, though)
43
Q

confabulates

A

remembers guesses as true memories (not purposefully lying, though)

44
Q

Alzheimer’s Disease

A
  • Severe memory loss associated with aging
  • Progressive, insidious
  • Strikes 50% of those over 85
  • Better procedural than declarative memory, e.g., can acquire new skills but don’t remember learning
  • Genetic components

—> person with Down’s syndrome (3 copies of chromosome 21) always acquire Alzheimer’s in middle age

—> genes on chromosome 14 and 1 related to early onset

—> genes on chromosome 10 and 19 related to late onset

45
Q

Alzheimer’s Disease cont. part 1

A
  • Environmental component

—> half of all cases have no known relatives with disease

—> Yoruba people of Nigeria have high-risk genes but lower incidence, maybe due to low-calorie, low fat, low salt diet

  • Brain proteins fold abnormally, clump together and interfere with normal neuronal activity
    plaques are structures formed from degenerating axons and dendrites (between cells)
    tangles are structures formed from degenerating structures within the soma (within cells)
    An abnormal protein called amyloid causes widespread degeneration of the brain (picture, page 388)
46
Q

plaques

A

are structures formed from degenerating axons and dendrites (HAS TO BE BETWEEN TWO CELLS)

47
Q

tangles

A

are structures formed from degenerating structures within the soma (ONLY WITHIN ONE CELL AT A TIME)

48
Q

amyloid

A
  • an abnormal protein
  • causes widespread degeneration of the brain (picture, page 388)
49
Q

Alzheimer’s Disease cont. part 2

A
  • Treatment

—> elevating levels of glucose can slightly enhance memory

—> drugs that increase acetylcholine activity increase some aspects of memory

—> diet rich in antioxidants has shown small effects

—> These can all slow the progression somewhat, but by no means do we have an effective treatment or cure

50
Q

Aplysia and the Study of Learning

A
  • D.O. Hebb proposed that when an axon successfully stimulates a cell it will be even more successful in the future
  • Hard to study this kind of thing in humans!
51
Q

Aplysia

A
  • a marine invertebrate, is a popular experimental animal

—> has few neurons, and they’re large, so it is easy to study behavior change as a result of neuronal activity

—> For example, touch results in the withdrawal of the gill
often study the withdrawal response and learning

52
Q

Aplysia and the Study of Learning cont [placeholder]

A

.

53
Q

Habituation

A
  • a decrease in response to a stimulus that is presented repeatedly and accompanied by no other change in stimuli

—> after repeated stimulation of gills the sensory neuron no longer increases action potentials to stimulate motor neuron

—> It’s believed this is due to a change in the synaptic activity b/t the sensory and motor neuron

54
Q

Sensitization

A
  • an increase in response to mild stimuli as a result of previous exposure to more intense stimuli

—> an increase in response to mild stimuli as a result of previous exposure to more intense stimuli

Thus, changes in synaptic activity produce learning

55
Q

Long-term Potentiation (LTP) and Depression (LTD) [placeholder]

A

.

56
Q

LTP

A
  • a burst of stimulation from axons, e.g., 100 excitations per second for 1-4 seconds, onto dendrites results in those synapses being even more responsive to similar input for minutes, days or weeks
  • We call the more responsive synapses “potentiated”
  • Three properties of LTP:
57
Q

specificity

A

only active synapses become strengthened

58
Q

cooperativity

A
  • nearly simultaneous stimulation by two or more axons results in LTP more strongly than repeated stimulation by just one
59
Q

associativity

A

pairing a weak input with a strong input enhances later response to the weak input

60
Q

LTD

A
  • Essentially forgetting
  • prolonged decrease in response to a synaptic input where two or more axons have been active together at 1-4 times per second – that’s not very often, so the synapse is weakened
61
Q

Biochemical Mechanisms of LTP in Hippocampus

A
  • Again, LTP has been VERY difficult to study, but let’s pin down what we (think we!) know
  • LTP only happens at glutamate synapses
  • Remember, we have different types of receptors (e.g., we have DA1, DA2 and DA 3 dopamine receptors)
  • Same goes for glutamate, except they are named differently
  • AMPA and NMDA glutamate receptors are the ones involved in LTP

—> open channels in postsynaptic neurons to let in one or more kinds of ions

—> On the AMPA receptors, glutamate opens sodium channels - similar to what we have studied

62
Q

Biochemical Mechanisms of LTP in Hippocampus cont part 2

A
  • NMDA receptors: channels are normally blocked by magnesium+ but Mg+ gets bumped when the AMPA receptors are stimulated by glutamate
  • Now that the NMDA channel is open, both Na and Ca enter
  • When calcium enters, it activates a protein called CaMKII, which is necessary for LTP, and sets several processes in motion:

—> structure of AMPA receptors change, becoming more responsive to glutamate

—> some NMDA receptors change to AMPA receptors and increase their responsiveness to glutamate

—> dendrites may build more AMPA receptors and make more branches

—> To summarize – it makes it easier for the post-synaptic cell to fire!

  • Once established, LTP no longer depends on NMDA synapses
63
Q

Biochemical Mechanisms of LTP in Hippocampus cont. part 3

A
  • Summary of LTP

—> A lot of glutamate stimulates AMPA receptors, and lots of positive sodium enters

—> The postsynaptic cell becomes depolarized, which pops the magnesium off and now the NMDA receptor’s channels are open

—> Calcium enters through the NMDA receptors and activates CaMKII

—> The CaMKII exerts changes in the postsynaptic cell that make it more responsive to future stimulation by glutamate: increasing # of AMPA receptors, increasing AMPA receptors’ responsiveness

—> The NMDA receptors were necessary to let the calcium in, but they don’t become potentiated, just the AMPA

64
Q

Biochemical Mechanisms of LTP in Hippocampus cont. part 4

A
  • Why are we talking about this again?
  • We think that LTP is involved in the consolidation of things into long term memory

—> following training on a memory task, LTP seen in hippocampus quickly and in cerebral cortex 90-180 minutes later

—> drugs that block NMDA receptors within 2 weeks of training also block consolidation of long-term memory

—> Mice with genes that cause abnormalities of the NMDA receptor learn slowly, and those with more than normal NMDA receptors have better memories

65
Q

LTP and Behavior cont.

A
  • Can drugs improve your memory?

—> gingko biloba sometimes produces small benefits in Alzheimer’s patients or others with circulatory problems by dilating blood vessels and increasing blood flow to the brain

—> no research on combination of “memory-boosting” supplements

—> A lot of “memory drugs” simply enhance your alertness through stimulant properties

—> Most of this stuff is NOT FDA regulated, so be careful!

66
Q

Facilitating Neuron

A
  • postsynaptic potentials evoked by an impulse are increased when that impulse closely follows a prior impulse

Psych 314 (11 decks)

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