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Neurobiology of Learning & Memory > Exam 3: Chapters 9-14 > Flashcards

Exam 3: Chapters 9-14 Flashcards

1
Q

Why is LTP not a memory?

A

LTP electrically induced in tissues slices or in the brain does not represent a behavioral experience.

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2
Q

What is inferred between the training phase and the testing phase?

A

The exsistence of a memory trace is inferred when the training experience influences behavior.

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3
Q

How can you determine if a change is due to influencing memory?

A

Before one can conclude that a biological manipulation infleunced memory, one has to be sure that it did not influence some other component of behavior.

Ex: sensory, attentional, motor, emotional, etc

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4
Q

What is the retention interval?

A

How long after training you test

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5
Q

What are the 3 dimensions that memory traces can differ?

A
  1. Duration (Short-term vs. Long term)
  2. State (Active state vs. Inactive)
  3. Vulnerability to disruption
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6
Q

What are the 2 important implications from the dimensions of memory traces?

A
  1. Memories become resistant to disruption as they age
  2. Memories in the active state are more vunerable to disruption that memories that have become inactive
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7
Q

What is the concept of consolidation?

A

The concept of consolidation exsists to explain the observation that newly formed memories are more easily disrupted compared to older ones.

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8
Q

How did electroconvulsive shock therapy affect the concept of consolidation?

How discovered ECS?

A

Cerletti and Bini applied electrical current across the brain to treat severe psychiatric disorders and it was discovered that the patients had impaired memories.

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9
Q

Explain the floor effect.

A

When a treatment is hypothesized to impair the memory processes that produce avoidance behavior, but the performance measure was too low to be further reduced by the drug.

The test is too hard to preform well.

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10
Q

What did Carl Duncan do and what did it show?

A

Carl Duncan was the first person to use ECS to experimentally induce amnesia in animals. He found that when ECS was administered within a minute after the training it produced amnesia, but not when given an hour after training.

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11
Q

What were the 2 theories about why ECS caused memory impairment?

A

Storage failure vs Retrieval failure

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12
Q

Describe Inhibitory Avoidance Conditioning.

A

Mice are nocturnal and have a desire to be in the dark. Mice were shocked when they tried to go into the dark and the memory could be traced by how long the mice avoided going to the dark.

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13
Q

Describe fear conditioning.

A

Mice exhibited a freeze response after associating a sound or environment with being shocked.

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14
Q

Describe the Morris Water-Escape Task.

A

Mice are placed in a tank and must find a platform. The time it takes to find the platform is tracked to determine how well the mouse remembers.

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15
Q

Describe Recognititon Memory Tasks.

A

In each task the rodent demonstrates that it remembers the training experience by exploring the new object more than the remembered object.

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16
Q

What is genetic engineering?

A

DNA is injected into a pronucleus from a fertilized egg and be designed to replace or knock out a particular gene.

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17
Q

What is optogenetics?

A

After rhospsin genes have been expressed on the membrane through genetic engineering, they can be activated by light to excite or inhibit neurons.

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18
Q

What must NMDA receptors have?

A

Functional NMDA receptors require a GluN1 subunit.

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19
Q

Describe Tonegawa’s experiment and the results.

A

Tonegawa’s group delted the GluN1 subunit in CA1. LTP could not be induced in the CA1 region, but could be induced in the dentate gyrus.

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20
Q

How do CA1-GluN1 KO mice preform in the Morris water maze?

A

CA1-GluN1 KO mice are impaired in learning the Morris water maze.

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21
Q

Morris was the first to find a possible role for NMDA receptors in memory formation. What was his essential methodology?

A

He implanted a cannular into a ventricle to deliver an NMDA receptor antagonist. He assessed the effect by studying its effect on the hidden platform version of the water task.

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22
Q

Describe the composition of the NMDA receptor.

A

Each receptor has four subunits, and they are some combination of the two classes GluN1 and GluN2.

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23
Q

How do CA3-GluN1KO mice prefrom in the Morris water maze?

What does this show about the role of NMDA receptors in CA3?

A

CA3-GluN1 KO mice do learn the maze when keeping the platform same over trials, but do not learn with new locations each day. This shows that the NMDA receptors in CA3 have a role in rapid learning.

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24
Q

What was Joe Tsien’s experiment?

Doogie mice.

A

Joe Tsien’s group overexpressed GluN2B subunits in the hippocampus and cortex of adult mice. This showed enhanced LTP to weak stimulus.

The mice preformed better in memory tests

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25
Q

What are the differences in subunit composition between juvenile and adults?

What is unique about the junevile receptors?

A

Juveniles have more GluN1-GluN2B receptors which stay open longer allowing more Ca2+ to enter. Adults have a higher ratio of Glu-N1-GluN2A.

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26
Q

How does the timing of CNQX affect preformance in the novel object task ?

CNQX is an AMPA antagonist.

A
  • CNQX before training blocks novel object memory formation
  • CNQX before testing blocks novel object memory retrieval
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27
Q

Describe Malinow’s experiment set up.

A

Malinow genetically engineered GluA1 AMPAr that fluoresced a green protein when brought to the membrane surface. He used a viral vector to deliver these receptors into the neurons in the amygdala. He exposed mice to a fear conditioning of paired and unpaired tone & shock.

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28
Q

Describe Malinow’s experiment results.

A

Fear conditioning drives AMPA receptors into the synapse and they are necessary for memory.

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29
Q

What was Malinow’s second experiment?

A

In the second experiment he asked if trafficking of GluA1s was necessary for the expression of conditioned fear. The rationale was that if they were necessary and the dummy receptors competed with the endogenous ones then the animals should display reduced LTP.

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30
Q

What is an AMPAkines?

A

AMPAkines keep the channel open longer, allowing more ions to enter and the synaptic response is enhanced to promote learning.

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31
Q

What was the result of using APV on a mouse in the food maze before training or before retrievall?

APV blocks NMDA.

A
  • APV injected before acquisition decreased learning
  • APV injected before retrieval had no effect on memory
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32
Q

What was the result of using CNQX on a mouse in the food maze before training or before retrievall?

CNQX blocks AMPA

A
  • CNQX injected before aquisition prevented learning
  • CNQX injected before retrieval prevented memory of correct spot
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33
Q

What are the effects shown in CaMKII KO mice?

A

LTP cannot be induced in CaMKII KO mice.

Mice could not learn the location of the hidden platform

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34
Q

How did fear learning change CamKII phosphorylation in the amygdala?

A

After fear learning there is an increase in CaMKII phosphorylation in the amygdala.

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35
Q

What is KN-62 and what did it do?

A

KN-62 inhibts phosphorylation of CaMKII and impaired both contextual and tone-fear conditioning.

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36
Q

Why is autophosphorylation of CaMKII important in fear learning?

A

Autophosphorylation is critical for rapid formation of a fear memory but it is not essential for memories produced with multiple training trials.

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37
Q

What happens when you inhibit the autophosphorylation of CaMKII?

A

Mice with defective autophosphorylation required several pairings to aquire the fear memory, whereas control mice acquired fear after only one pairing.

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38
Q

What are the roles of actin polymerization in object-place memory?

What happens when you block + what is Cofilin’s role

A
  • Blocking actin polymerization in hippocampus blocks object-place memory formation
  • Phosphorylated cofilin (allows actin polymerization) increases in hippocampus following object-place learning
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39
Q

What happens in the insular coretex during Conditioned Taste Aversion?

What happens when you block actin polymerization?

A
  • PSD size (actin polymerization) increases in insular cortex after conditioned taste aversion
  • Blocking actin polymerization blocks CTA formation
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40
Q

What are the types of memory involved in the radial arm maze test?

A
  • Reference memory component: remembering which arms are always baited
  • Working memory component: remembering which arms it has already been too
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41
Q

GluA1 subunits are found on AMPA receptors

How are the different memory components affected in the radial arm maze by GluA1 KO?

What does this suggest about GluA1 receptors?

A

These mice can learn and remember the reference memory component, however they are impaired on the working memory component. This suggests that GluA1 receptors are critical for working memory.

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42
Q

What are the 3 important principles of memory consolidation?

A
  1. Enduring memories require behavioral experiences that generate new proteins
  2. These consolidation processes occur in multiple waves
  3. These processes are sustained by an autoregulatory positive feedback loop that ensures a continuous supply of synaptic mRNAs for local translation
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43
Q

How is a drug or gene’s effect on memory evaluted?

Pertaining to retention intervals

A

Assesing effect on memory at 2 retention intervals:
- A short interval (1-2 hours) designed to assess short-term memory
- A longer interval (~24 hours) designed to assess long-term memory

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44
Q

What happens when you inhibit protein synthesis shortly before or after training?

Anis (protein synthesis inhibitor)

A
  • Applied before training, Anis decreased LTM, but does not affect STM
  • Applied shortly after training, Anis decreases performance, however there is still memory which shows that protein synthesis occurs within the first 5 minutes after training
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45
Q

What happens when you inhibit protein syntheis long after training?

Anis (protein synthesis inhibitor)

A

-Protein synthesis is required for more then a day for a memory to persist longer than a week

46
Q

What is the difference between mTORC1 and mTORC2?

How do you inhibit mTORC2?

A

mTORC1 is sensitive to rapamycin, but mTORC2 is not. KO RICTOR gene is the only way to manipulate mTORC2.

47
Q

How do RICTOR KO mice differ in contextual fear?

What can it be rescued by?

A

When experiencing contextual fear conditioning, RICTOR KO mice display normal STM but impaired LTM. Impairment can be rescued by JPK that promotes actin polymerization.

48
Q

Why are LTM and LTP impaired in RICTOR KO mice?

A

The regulation of actin dynamics and signaling is disrupted in RICTOR KO mice. The ratio of F-actin to G-actin and phosphorylated Cofilin is reduced in RICTOR KO mice.

49
Q

What does mTORC1 do?

A

Removes the inhibitory influence of the TOP protein 4E-BP to intiate local protein synthesis.

50
Q

What does mTORC2 do?

A

Contributes to continuation of actin polymerization.

51
Q

When does BDNF protein levels peak after fear conditioning?

A

Peaks at both 1 hour and 12 hours after fear conditioning.

52
Q

What happens when you impair BDNF function 1 hour after training?

A

Impairs the fear response at both the 1 day and 7 day retention intervals.

53
Q

What happens when you impair BDNF function 9 hours after training?

A

Impairs the fear response only on the 7-day retention test.

54
Q

What is the role of the first and second BDNF peaks?

A
  • The first peak of BDNF is critical for the memory expressed on both the 1 day and 7 day retention tests
  • The second BDNF peak is required only to support the memory expressed on the 7 day retention test
55
Q

How does a behavioral experience lead to a memory?

A

A behavioral experience initiates a genomic signaling cascade that results in new plasticity products needed to consolidate the memory for the experience.

56
Q

How does hippocampal CREB antisense affect memory?

What kind of memory?

A

Has no effect on STM but blocks LTM

57
Q

When do you see increased levels of CREB?

How long do they remain high?

A
  • Increased levels of phosphorylated CREB are present in the hippocampus shortly after training and remain high for at least 20 hours
58
Q

When do you see increased levels of C/EBPb?

A

Increased levels of C/EBPb mRNA are not observed until 9 hours after training.

59
Q

How did C/EBPb antisense affect inhibitory avoidance memory?

A

C/EBPb antisense infused into the hippocampus 5 and 24 hours after training impaired retention of the inhibitory avoidance memory.

60
Q

Describe the BDNF positive feedback loop.

1. BDNF first wave activates what?
2. STM? LTM 2 days, 7 days?

A
61
Q

What is the potential role for sleep in memory consolidaiton?

A

During sleep, intrinsic neural activity reactivates the initial neural circuit with the conseqeunce that new proteins are synthesized from the replacement protein provided by the positive autoregulatory BDNF feedback loop to support the second wave of consolidation.

62
Q

What is the support for the role of sleep in memory consolidation?

A
  • Sleep deprivation impairs memory and impairs mTOR function
  • Restoring mTOR function rescues the sleep-deprived induced memory impairment
63
Q

What is the evidence that protein degradation contributes to memory consolidation?

A
  • Fear conditioning induces polyubiquitination of PSD scaffolding proteins, this process is prevented by NMDA antagonist
  • A proteasome inhibitor after training impairs both cued and contextual fear conditioning
64
Q

What are the 2 independent effects that experince has?

A
  1. It can initiate the acquisation and storage of the memory trace
  2. It can activate the release of adrenal hormones that can modulate the processes that store the memory
65
Q

What are memory modulators?

A

Hormonal and other neural systems that are not a part of the storage or retrieval system, but can influence the synapses that store the memory.

66
Q

Why do memory modulators have a time-limited role?

A
  • They influence only the storage of very recently acquired memories
  • They operate during a period of time shortly after the behavioral experience when the trace is being consolidated
67
Q

Describe McGaugh’s experiment and what the results suggested.

A
  • Inject a stimulant before and after training lead to enhanced learning, but injecting before the retention test had no effect.

These results suggested that there is a period of time following training when the processes that consolidate memory could be enhanced.

68
Q

What happended when amphetamine was injected after training?

What does this result show about the amygdala?

A

Improved retention performance; Amygdala facilitates storage of these memories but is not necessary to form the memory.

69
Q

What is the mediator of the amygdala’s modulatory effects?

What experiment proved this?

A

BLA is likely the mediator of the amygdala’s modulatory effects; An injection of lidocaine into the basolateral nucleus of the amygdala following training impaired retention

70
Q

What is the role of epinephrine in memory?

Describe the experiment.

A

On the training trial, rats recieved a mild shock. After training, rats were injected with Epi (to mimic what would naturally be released if the animals had recieved a strong shock). The mice displayed enhanced memory.

71
Q

Epinephrine does not cross the blood brain barrier.

How does Epinephrine affect the brain?

A
  1. Adrenal medulla releases Epi and it binds to the adrenergic receptors on the vagal nerve
  2. The vagal nerve will release glutamates on the neurons in the solitary tract nucleus (NTS)
  3. Activated NTS neurons release glutamate onto neurons in the locus coeruleus
  4. When activated the LC release Norepi that binds to receptors in the BLA
72
Q

What is microdialysis?

A

Allows extracellular fluid to be collected from deep within the brain using a probe implanted in the brain.

73
Q

What is the evidence that NE in BLA enhances memories?

A
  • Injection of NE into the Amygdala following training enhanced retention, but when NE antagonist was injected, the retention was impaired
74
Q

What is the molecular pathway when NE is released into the amygdala?

A

NAdR (metabotropic) –> cAMP –> PKA –> trafficking of GluA1 to extrasynaptic region –> sustained activity

75
Q

What does NE do when released into the Amygdala?

A
  • Activated BLA by NE releases glutamate onto Ca2+ storage site synapses
  • NE likely causes BLA neurons to give a sustained Glu releases that should boost the signaling pathways needed to strengthen the trace
76
Q

By what mechanism does the BLA modulate memories?

A

These results suggest that BLA might modulate memory by influencing the level of Arc protein in the hippocampus.

77
Q

What is bioenergenics?

What is the primary source of energy for the brain?

A

The flow of energy in cells

The primary source of energy is glucose that enters the brain

78
Q

Describe the Epi-Liver-Glucose connection for the importance of remembering stressful events.

A

An arousing event activates the adrenal medulla to release Epi into the blood system where it binds to receptors onto the liver. to release glucose into the blood to activate the fight-or flight sytem and provide the brain energy for transcription/translation in order to process the memory and consolidate it.

79
Q

How does Epi modulate memory?

How did we show this?

A

Epi modulates memory by binding to adrenergic receptors on the liver cells causing them to release glucose.

Injections of Epi or Glucose influence inhibitory avoidance memory strength in a dose-dependent manner.

80
Q

How does age affect underlying memory mechanisms?

What experiment showed this?

A

Underlying memory mechanisms may not be altered in aged rats, only a deficit in the neuro-adrenal hormonal modulatory system.

  • In response to an arousing event, Epi was released in boht young and old rats, but only young rats secreted glucose. If glucose is injected into older rats, phosphorylation is detected allowing for transcription and enduring memory.
81
Q

How do glucocorticoids affect memory?

What system does it work on?

A
  • When Dex (glucocorticoid agonist) is injected following traning it enhances retention
  • Amygdala NE antagonist prevents Dex from enhancing retention

Glucocorticoids likely exert their affects through LC NE

82
Q

What is the psychological view of forgetting?

Including interference and retreival failure.

A

A second learning event could produce amnesia for a prior experience by interfering with the consolidation of the first, if the second event was similar to the first and occurred shortly after. A competing memory can also interfere with the expression of the target memory (retrieval failure).

83
Q

What is the evidence for the active decay theory?

A

NMDA antagonists prevented forgetting, while vehicle rate forgot the task. An NMDA agonist also enhances forgetting because it promotes calcium entry.

84
Q

In regards to forgetting what happens after learning and the synapse is potentiated?

A

Molecular events intitated by small amounts of calcium actively de-potentiate the synapses that support the memory.

85
Q

What molecular event causes forgetting?

How do we know this?

A

Forgetting is due to the gradual removal of AMPA receptors.

Injection of a drug that prevents the removal of AMPA receptors, prevents forgetting.

86
Q

How do NMDA receptors bidirectionally control forgetting?

A
  • Selectively inhibitng GluN2B receptors prevented forgetting of the object’s location
  • An NMDA receptor agonist promotes rapid forgetting
87
Q

What is Calcineurin and how does it affect forgetting?

A

Calcineurin is a phosphatase activated by calcium. Inhibitng Calcineurin prevented forgetting as compared to a vehicle injection.

88
Q

What are some of the signaling events that lead to AMPA receptor endocytosis?

A
  1. Following the strengthing of synapses that support memory, there is tonic release of small amounts of Glu
  2. The leads to Ca2+ entering spine and activating the phosphatase Calcineurin, which dephosphorylated Stargazin and other targets
  3. AMPA receptors are liberated from PSD-95 traps, allowing for their endocytosis.
89
Q

How does the state of Rac1 determine the rate of forgetting?

What is Rac1?

Retention of context fear memory was poor if multiple shocks were separted by 12 seocnds. Space repetitions (120 seconds) of the shock resulted in no forgetting.

A

Rac1 is part of the Rho family of GTPases that contribute to the regulation of actin
- When Rac1 was inhibited, forgetting was prevented in aminals in the 12-second contions, and when Rac1 was activated, animals in the 120-second condition forgot the fear memory

90
Q

How does activation of Rac1 affect spines?

A

Activating Rac1 can shrink spines that have been enlarged from training and results in forgetting.

91
Q

Describe the charcteristics of PKMz. What are the 3 roles of PKMz?

A
  • No regulatory unit
  • mRNA is present in dendrites
  • Self perpetuates
    1. Releases pools of GluA2s
    2. Inhibits the GluA2 endocytosis
    3. Clutsters PSD-95
92
Q

What were the effects on spaitial memory when you interferred with PKMz?

ZIP reverses the effects of PKMz.

A

Interfering with PKMz erases spatial memory.

Saline mice avoid where shocks were more than ZIP mice.

93
Q

What were the effects on taste aversion when you interferred with PKMz?

ZIP reverses the effects of PKMz.

A

A single injection of ZIP into the insular cortex will greatly reduce a well consolidated taste-aversion memory.

94
Q

What were the effects on memory when you overexpressed PKMz?

A

Enhancing PKMz in the insular cortex 5 days prior to training enhanced memory for that experince because it converted a weak memory into a strong one.

95
Q

How does PKMz counter forgetting?

What showed this?

A

PKMz counters forgetting by preventing AMPA receptor endocytosis.

Infusing ZIP into the basolateral amygdala resulted in forgetting, however if GluR23Y (blocks endocytosis of AMPA receptors) was also infused, fogetting was prevented.

96
Q

What are the 4 properties an engram must have?

A
  1. A change in the brain from a specific experience.
  2. Has the potentional for retrieval
  3. Content reflects what transpired at encoding and predicts what can be recovered during retrieval
  4. May exist in a dormant state between the 2 active processes of encoding and retrieval
97
Q

According to Richard Semon, what is an engram?

A

The engram is not the memory but provides a physical basis for it.

98
Q

To conclude that neurons belong to an engram, what must the researcher prove?

A
  1. Be able to tag cells activated by the behavioral experience
  2. Demonstrate that some of those cells are also activated by the memory test
  3. Direct activation of these cells generates the appropriate behavior
  4. Inhibiting these specific cells prevents the occurence of the appropriate behaviors
99
Q

How is Arc used to tag neurons?

Arc is an immediate early gene

A

Arc is rapidly transcribed in the nucleus in repsonse to a learning event, Arc very quickly translocates to the cytoplasm. Thus, if the same neuron is activated by both experinces, Arc should be present in both its nucleus and the cytoplasm, whereas cells activated by only the first or second experinece would have Arc only in either the nucleus of the cytoplasm.

  • Experinces relate to a rat exploring the same environment on 2 different occasions.
100
Q

Explain the TetTag mouse model.

A

The TetTag mouse is genetically engineered so that LAC will be expressed only in cells that are activate at a particular time. Temporal control of expression of LAC is regulated through a tTA ON system, as long as DOX is in the animal’s drinking water (tTA OFF), the tTA system cannot drive LAC expression.

  • LAC is expressed in cells tagged during the tTA ON period (kind of like labeling neurons)
101
Q

How does the TetTage mouse model demonstrate engrams in the presense of fear conditioning?

A

Fear conditioning takes place with DOX removed, and cells that are activae during this period are tagged with LAC. Cells that are active during the retrieval test briefly express the IEG ZIF. Cells tagged with both LAC and the IEG marker ZIF are considered engram cells because they were activated by both the conditioning experience and the retrieval test.

102
Q

How has optogenetics been used to activate engram cells?

A

Mice were habituated to context A with DOX in drinking water (ie no labeling), the conditioned to context B with shock and with DOX removed. This allowed the tTA system to drive the expression of ChR2 in cells that were active during contextual fear conditioning. When blue light was applied to neurons expressing ChR2, the mice displayed freezing behavior in the unshocked context.

103
Q

How does sleep / repetitive synchronous activity amond subassemblies allow engrams to survive?

A

Mice were genetically engineered so that cells activated by context exploration switched from fluorescing green to fluorescing red. During sleep some of the red subassemblies replayed. During the retrieval period when mice were returned to the context, only subassemblies that were replayed during sleep were activated.
* Therefore, repetitive synchronous activity among subensembles allows an engram to survive through post learning and provide a basis for contextual retrieval.

104
Q

What is the importance of CREB in rescuing impaired long-term memory?

A

Injecting a virus that overexpresses CREB into the lateral amygdala prior to the conditioning trials can eliminate the imparied long-term memory normally found when the trial time was short intervals.

105
Q

How do neurons that overexpress CREB become engram cells?

A

(a) neurons in the lateral amygdala compete to participate in the neuron ensemble that supports the fear memory and
(b) neurons expressing high levels of CREB at the time of fear conditioning win the competetion

106
Q

How does CREB’s affect on neuronal excitability influence engram cells?

A

CREB increases neuronal excitability. Neuronal inputs to these high CREB neurons may causes an action potential. Because potential engram cells are reciprocally inhibiotry, the CREB-expressing cells will inhibit other cells and prevent them from becoming engram cells.

107
Q

Why did Brian Derrick conclude that the activation NMDA receptors during the retention interval produces forgetting?

A

He gave rats daily injections of an NMDA agonists and found that it prevented the decay of LTP and the forgetting of a working memory task.

108
Q

What might be the important brain adaptation that is responsible for why we forget?

A

Processes that produce active forgetting at psychological level may have evolved to help maintain the balance of excitatory and inhibitory inputs on a neuron.

109
Q

The study of neural dynamics by Inokuci’s group (Gandour et al.) revealed several important discoveries. Describe two.

A
  1. Not all ensembles activate by the learning experience were activated by the retrieval test.
  2. Only ensembles active during sleep became were activated by retrieval.
110
Q

Why would one vary the interval separating training and the administration of a protein synthesis inhibitor such as anisomycin?

A

This would be done to be sure that the effect was selective for proteins synthesized in response to the memory-inducing behavioral experience and not just a nonselective effect of blocking protein synthesis.

111
Q

Describe two sources of evidence that BDNF is important for memory consolidation.

A

1) BDNF protein levels are increased in the hippocampus by contextual fear conditioning and place learning and in the BLA by fear conditioning.
2) 2) Interfering with BDNF function impaired the development of long-term memory.

112
Q

What were the results of injecting lidocaine or clenbuterol into the BLA?

A

Lidocaine reduced the level of Arc protein in the hippocampus and the memory experience was impaired. Clenbuterol increased the level of Arc protein in the hippocampus, and the memory for the training experience was strengthened.

Neurobiology of Learning & Memory (5 decks)

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