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Neurobiology -BIOL4370 > Lecture 2- Learning and Memory > Flashcards

Lecture 2- Learning and Memory Flashcards

1
Q

What are the two general types of memory

A
  1. Declarative memory involves conscious recall of facts and events,
  2. Non-declarative memory is unconscious and includes procedural memory and skills
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2
Q

What are examples of nondeclarative memory?

A
  1. Motor skills (e.g., riding a bike)
  2. Associations (e.g., classical conditioning like Pavlov’s dog)
  3. Priming cues (e.g., quicker recognition of words you’ve seen recently)
  4. Puzzle-solving skills (e.g., solving a jigsaw puzzle without recalling previous steps)
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3
Q

What demonstrates the evolutionary conservation of memory?

A

The instinctive crouching of young birds at the sight of a predator silhouette demonstrates evolutionary conserved memory responses

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4
Q

How are evolutionarily conserved memories linked to brain processes?

A

These memories involve instinctive behaviors that must have cellular and molecular processes involved in the brain, possibly through epigenetic mechanisms.

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5
Q

What happens in the monkey pulvinar neurons when exposed to snake images compared to other stimuli?

A

Monkey pulvinar neurons show increased spiking when exposed to snake images compared to other stimuli, indicating an exaggerated neural response to a potential threat

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6
Q

How does the response time of monkey pulvinar neurons to snake images compare to other stimuli?

A

The response time of monkey pulvinar neurons to snake images is faster compared to other stimuli, indicating a quicker reaction to perceived threats.

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7
Q

What was the hypothesis and conclusion of Lashley’s 1920s studies on maze learning in rats regarding memory storage?

A

Hypothesized that memory is not localized but distributed throughout the cortex, a concept known as “equipotentiality.”
- Conclusion (incorrect): memory centers do not exist

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8
Q

What principle did Lashley’s 1950s lesion studies support, and what was observed?

A

Lashley’s studies supported the “mass action principle,” observing that the more complex the task, the greater the impact of cortical lesions on learning and memory.

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9
Q

What are the two forms of non-associative learning described in Aplysia and what do they signify?

A

The two forms of non-associative learning are habituation (decreased response to repeated stimuli) and sensitization (increased response to a stimulus), exemplify two different forms of learning/memory, mediated by the same set of cells.

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10
Q

What happens to the Aplysia’s gill-withdrawal reflex with repeated stimulation of the siphon?

A

With repeated stimulation, the Aplysia’s gill-withdrawal reflex decreases in magnitude (becomes weaker and less intense over time), demonstrating short-term habituation.

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11
Q

What initiates short-term sensitization in Aplysia’s gill withdrawal reflex?

A

A short-term sensitization is initiated by a tail shock, which leads to an increased reflex response to touch.

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12
Q

How is long-term sensitization achieved in Aplysia’s gill withdrawal reflex?

A

Long-term sensitization is achieved through repeated tail shocks over several days, where the gill-withdrawal reflex is enhanced over time.

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13
Q

Describe the roles of glutamate and GABA in synaptic transmission.

A

Glutamate: Acts as an excitatory neurotransmitter, causing the postsynaptic neuron to fire.

GABA: Acts as an inhibitory neurotransmitter, preventing the postsynaptic neuron from firing.

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14
Q

What is the role of serotonin in short-term sensitization?

A

Serotonin increases glutamate release from the presynaptic sensory neuron, which enhances the stimulation of the postsynaptic motor neuron, leading to stronger gill withdrawal.

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15
Q

What is the common process that leads to gill withdrawal in both short-term and long-term sensitization?

A
  • Sensitizing stimulus triggers serotonin release from the modulatory neuron.
  • Serotonin boosts glutamate release from the sensory neuron.
  • Glutamate stimulates the motor neuron, leading to gill muscle contraction and withdrawal
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16
Q

What happens inside the sensory neuron after serotonin is released? - internal mechanism the mechanism that causes the sensory neuron to release more glutamate.

A
  • Serotonin binds to receptors on sensory neuron.
  • This increases cAMP inside the neuron, which activates PKA.
    (Protein Kinase A).
  • PKA helps the sensory neuron release more glutamate, leading to stronger activation of the motor neuron.
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17
Q

How do short-term and long-term sensitization differ in terms of neuron changes?

A
  • In short-term sensitization, the effect is temporary with no lasting changes inside the neuron.
  • In long-term sensitization, repeated stimuli cause increased serotonin release, which activates cAMP and PKA, leading to gene expression changes and synapse growth, creating lasting effects.
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18
Q

What changes occur inside the sensory neuron during long-term sensitization?

A
  • Repeated serotonin release increases cAMP.
  • cAMP activates PKA (Protein Kinase A).
  • PKA moves to the nucleus of the sensory neuron.
  • PKA triggers changes in gene expression.
  • New proteins are produced.
  • These proteins strengthen synapses, leading to longer-lasting responses.
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19
Q

What are metabotropic glutamate receptors and how do they differ from ion channels?

A

They activate intracellular signaling cascades that modulate synaptic and cellular functions instead of allowing ions to pass directly.

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20
Q

What are the steps involved in the signaling cascade for short-term sensitization? -this describes how the signal starts from serotonin binding outside the neuron and leads to internal changes that ultimately result in the release of glutamate, which enhances communication between neurons.

A
  • Serotonin (5-HT) binds to its receptor.
  • Adenylate cyclase (AC) is activated, increasing cAMP levels.
  • cAMP promotes the dissociation of PKA regulatory subunits.
    PKA blocks potassium (K+) channels.
  • Depolarization activates voltage-dependent calcium (Ca2+) channels.
  • Calcium influx triggers the release of glutamate, enhancing synaptic transmission.
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21
Q

What are the steps involved in the signaling cascade for long-term sensitization?

A
  • Serotonin (5-HT) binds to its receptor.
  • Adenylate cyclase (AC) is activated, increasing cAMP levels.
  • cAMP promotes the dissociation of PKA regulatory subunits, activating PKA.
  • PKA activates transcription factors, including CREB.
  • CREB promotes the synthesis of ubiquitin hydrolase (UH) and pro-synaptogenic signals.
  • UH degrades the regulatory subunits of PKA, keeping PKA persistently active.
  • Persistent activation of PKA leads to long-term changes in synaptic strength, resulting in long-term sensitization.
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22
Q

What are pro-synaptogenic signals?

A

Pro-synaptogenic signals strengthen and build synapses, improving neuron communication for learning and memory.

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23
Q

What are the main components of the tri-synaptic hippocampal circuit, and what are their roles?

A

The components are:
1. Entorhinal cortex - Input to the hippocampus via the preforant path
2. Dentate gyrus - Responsible for pattern separation, projects via mossy fiber pathway to CA3
3. CA3 - Handles pattern completion, Projects via Schaffer Collateral pathway to CA1
4. CA1 - Processes spatial and contextual memory.

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24
Q

What role do the Dunce, Rutabaga, and Amnesiac genes play in memory in fruit flies?

A
  1. Dunce: Breaks down cAMP
  2. Rutabaga: Helps produce cAMP
  3. Amnesiac: Connects signals to adenyl cyclase (affects cAMP production).
  4. Impact of Mutations: Impair memory in fruit flies.
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25
Q

How are experiences represented at the cellular level in the brain?

A

Experiences are represented at the cellular level by increased efficacy of synapses, which is proportional to the degree of correlation between pre- and post-synaptic activity.

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26
Q

How was LTP demonstrated by Bliss and Lomo in 1973?

A

Bliss and Lomo showed LTP in 1973 by repeatedly stimulating neurons in anesthetized rabbits, which made synaptic responses stronger and kept them enhanced for hours. This proved that synaptic strength can last a long time.

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27
Q

What occurs during Early-LTP?

A

During Early-LTP, tetanic stimulation leads to a temporary increase in synaptic strength due to the activation and phosphorylation of AMPA receptors, representing short-term memory.

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28
Q

What does Early-LTP represent in terms of memory?

A

Early-LTP is an analog for short-term memory because the synaptic increase is transient and does not last long.

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29
Q

How does late-LTP contribute to long-term memory and distinguish itself from early-LTP?

A

Late-LTP, triggered by repeated tetanic stimulation, involves phosphorylation of AMPA receptors and protein synthesis, leading to sustained synaptic strengthening essential for long-term memory.

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30
Q

How might the reduction of Mdga2 affect synaptic mechanisms involved in LTP?

A

Reducing MDGA2 could weaken excitatory synapses, making it harder to maintain LTP and form memories, because MDGA2 helps keep these synapses stable and strong.

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31
Q

What are the roles of NMDA and AMPA receptors in LTP?

A

In LTP, NMDA receptors are involved in controlling calcium influx that initiates synaptic changes, while AMPA receptors increase the synaptic current and contribute to stronger synaptic responses.

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32
Q

What are the key properties of LTP? -These describe the broader behavior of synaptic strengthening when it does occur.

A

The four key properties of LTP are:
1. Associativity
2. Cooperativity
3. Specificity
4. Enduring

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33
Q

What is Associativity in LTP?

A

Associativity requires simultaneous activation of multiple synapses to trigger depolarization.

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34
Q

What is Cooperativity in LTP?

A

Cooperativity requires both pre- and postsynaptic neurons to be active for LTP to happen. This involves Hebbian learning, where the connection between neurons strengthens when they are active at the same time (“cells that fire together, wire together”).

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35
Q

What is Specificity in LTP?

A

Specificity explains how only active synapses undergo potentiation (become stronger) during LTP while inactive ones stay the same.

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36
Q

What does it mean that LTP is Enduring?

A

LTP changes are long-lasting; some memories can persist for over 80 years due to these mechanisms.

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37
Q

What do NMDA receptors mediate in LTP?

A

NMDA receptors mediate the induction of LTP by allowing calcium ions (Ca²⁺) to enter the postsyanptic neuron once depolarization removes magnesium ions (Mg²⁺) from the receptor.

38
Q

How do AMPA receptors maintain LTP?

A

AMPA receptors maintain LTP through phosphorylation, which increases the number of AMPA receptors at the synapse, leading to their insertion into the membrane and strengthening synaptic connections, which helps maintain LTP.

39
Q

What are the key steps in long-term potentiation (LTP) signaling?

A
  1. NMDA receptor activation: Triggers the process by allowing calcium (Ca²⁺) into the neuron.
  2. Increased postsynaptic Ca²⁺: Calcium levels rise inside the postsynaptic neuron.
  3. Activation of CaMKII and PKC: These proteins are activated by the increase in calcium.
  4. Phosphorylation of AMPA receptors: AMPA receptors are modified by adding phosphate groups.
  5. AMPAR trafficking to the synaptic membrane: AMPA receptors move to the synapse.
  6. Stabilization of postsynaptic AMPARs: AMPA receptors stay at the synapse, strengthening the connection.
40
Q

What does long-lasting LTP require to support synaptic modifications?

A

Long-lasting LTP requires protein synthesis and transcriptional programs to maintain and support long-term synaptic modifications. without it, LTP decays.

41
Q

What happens to LTP when protein synthesis is inhibited?

A

When protein synthesis is inhibited, LTP decays, indicating that new protein synthesis is necessary for long-term synaptic changes.

42
Q

How do transcriptional programs contribute to LTP?

A

Transcriptional programs regulate gene expression, producing the proteins needed to maintain long-lasting synaptic changes during LTP.

43
Q

What role do epigenetic modifications play in LTP?

A

Epigenetic modifications may help sustain long-term synaptic changes during LTP by altering gene expression without changing the DNA sequence.

44
Q

What is LTD associated with? How is it induced?

A
  • Associated with a loss of synaptic AMPA receptors.
  • Low-frequency stimulation of the Schaffer collateral axons triggers LTD.
44
Q

What is LTD in the context of synaptic transmission?

A

Long-term depression (LTD) is a process that leads to a long-lasting weakening (depression) of synaptic transmission.

45
Q

What role does Ca²⁺ play in LTD?

A

A low-amplitude rise in Ca²⁺ concentration in the postsynaptic CA1 neuron activates protein phosphatases, which remove AMPA receptors from the synapse, weakening the synapse.

46
Q

What is the key factor that differentiates LTP from LTD in terms of calcium?

A

LTP requires transient, high levels of Ca²⁺, while LTD requires tonic, low levels of Ca²⁺.

47
Q

How do kinases and phosphatases differ in their roles in LTP and LTD?

A

-Kinases, activated by high Ca²⁺ levels, phosphorylate synaptic proteins to induce LTP.
- Phosphatases, activated by low Ca²⁺ levels, dephosphorylate proteins, leading to LTD.

48
Q

How is memory formation linked to synaptic transmission in rats?

A

Memory formation is associated with the potentiation of synaptic transmission, meaning that synapses strengthen as the rat learns to avoid the dark compartment where it receives shocks.

49
Q

What frequencies of stimulation produce LTP and LTD in human brain slices?

A

Low-frequency stimulation (1 Hz) produces long-term depression (LTD), weakening synaptic strength, while high-frequency stimulation (100 Hz) produces long-term potentiation (LTP), strengthening synaptic connections.

50
Q

What happens when NR1 is knocked out in the CA1 region of the brain, and does it affect LTP in other regions?

A

Knocking out NR1 in the CA1 region blocks long-term potentiation (LTP) in that area, preventing synaptic strengthening. However, this does not affect LTP in the dentate gyrus (DG).

51
Q

Why is it important that LTP is not affected in the dentate gyrus (DG) when NR1 is knocked out in CA1?

A

It shows that different hippocampal regions work independently. Even if LTP is blocked in CA1, the DG can still support synaptic strengthening, indicating that memory formation has multiple pathways as a backup for learning.

52
Q

What is contextual fear conditioning (CFC)?

A

CFC is a test of memory where rodents associate a specific context with a mild shock and later freeze when placed back in the same environment, indicating memory retention.

53
Q

How is memory strength measured in contextual fear conditioning?

A

Memory strength is measured by how long the rodents remain immobile (freezing) when placed back in the context where they previously received a shock.

54
Q

What is the Morris Water Maze used for?

A

The Morris Water Maze is used to test spatial memory in rodents by measuring how quickly they find a hidden platform in a pool using visual cues.

55
Q

How is memory strength measured in the Morris Water Maze?

A

Memory strength is measured by the latency (time taken) to find the hidden platform, with faster times indicating stronger memory.

56
Q

What part of the brain is required for the Morris Water Maze task?

A

The hippocampus, specifically NMDA receptors, is required for spatial memory tasks like the Morris Water Maze because NMDA receptors help initiate learning by allowing synaptic changes.

57
Q

What happens when NMDA receptors are blocked during spatial memory tasks?

A

Blocking NMDA receptors with an antagonist like APV impairs both long-term potentiation (LTP) and spatial memory formation, making it harder for subjects to learn and remember the task.

58
Q

How does APV injection affect LTP in the dentate gyrus?

A

APV injection reduces LTP in the dentate gyrus, which weakens synaptic plasticity necessary for memory formation.

59
Q

What is a probe trial in the Morris Water Maze used for?

A

A probe trial tests memory retention by removing the platform and measuring how much time the animal spends in the correct quadrant, where the platform was previously located.

60
Q

How does blocking NMDA receptors affect performance in the Morris Water Maze probe trial?

A

Blocking NMDA receptors with APV results in a loss of memory for the correct quadrant, showing that NMDA receptors are essential for retaining spatial memory

61
Q

What effect does overexpresion of NR2B have on memory and LTP?

A

Overexpression of NR2B in the “Doogie mouse” enhances long-term potentiation (LTP) and improves memory, making the mouse perform better in memory tasks like fear conditioning.

62
Q

What is the role of CaMKII in memory?

A

CaMKII is activated after NMDA receptor stimulation and phosphorylates AMPA receptors, helping to strengthen synapses and promote memory formation.

63
Q

How does CaMKII interact with AMPA receptors?

A

CaMKII phosphorylates AMPA receptors, helping them move to the synapse, which strengthens communication between neurons and supports memory retention.

64
Q

What happens to learning and memory in CaMKII knockout (KO) mice in the Morris Water Maze?

A

learning and memory are impaired. They take longer to find the platform and spend less time in the correct area, showing weaker spatial memory.

65
Q

What are hippocampal place cells, and how do they function in navigation?

A

Place cells in the hippocampus fire in response to specific locations, creating spatial maps and helping animals remember their position as they navigate.

66
Q

How do hippocampal place cells function in humans?

A

In humans, hippocampal place cells are active during spatial navigation tasks, as seen through increased hippocampal activity during virtual environment navigation.

67
Q

How does navigation experience affect the hippocampus in taxi drivers?

A

Extensive navigation experience, like in taxi drivers, leads to growth in the posterior hippocampus, which is involved in spatial memory and navigation.

68
Q

What is the cognitive map theory of the hippocampus?

A

Suggests the hippocampus forms a map of the spatial environment, with grid cells in the entorhinal cortex firing in patterns that create a grid of the environment.

69
Q

What is immediate memory?

A

Immediate memory lasts for a few seconds and stores sensory information, acting as a brief memory register for each sensory modality.

70
Q

What is working memory?

A

Working memory holds and manipulates information for seconds to minutes and is essential for goal-directed behavior

71
Q

What is long-term memory?

A

Long-term memory can last from days to years and is likely stored across the cortex, depending on enduring changes in synaptic strength.

72
Q

What is the order of information flow in the medial temporal lobe memory system?

A

Information flows from the neocortex to the perirhinal and postrhinal cortices, then to the entorhinal cortex, and finally to the hippocampus.

73
Q

What is the medial temporal lobe memory system?

A

The medial temporal lobe memory system includes the hippocampus, entorhinal cortex, and related regions, and it processes and transfers information to long-term memory.

74
Q

What evidence supports the role of the medial temporal lobe in memory?

A

Wilder Penfield’s research showed that electrical stimulation of the medial temporal lobe causes patients to experience sensations of past experiences, providing evidence of the region’s role in memory recall.

75
Q

What did microelectrode studies in epileptic brain tissue reveal about memory in the medial temporal lobe?

A

Microelectrode studies revealed that neurons in the medial temporal lobe preferentially responded to categories of objects such as faces, household items, and outdoor scenes.

76
Q

What are the two types of memory consolidation processes?

A
  1. Synaptic consolidation, where memories are represented by long-term changes in synaptic strength
  2. Systems consolidation, where memories are gradually moved over time to distributed locations throughout the neocortex.
77
Q

How does memory retrieval relate to the conditions during encoding?

A

Memory retrieval is stronger when the conditions during retrieval are similar to those at encoding, as the same brain regions are activated.

78
Q

What is retrograde amnesia?

A

Retrograde amnesia is the loss of past memories, typically occurring before the time of trauma, while new memories can still be formed.

79
Q

What is anterograde amnesia?

A

Anterograde amnesia is the inability to form new memories after a trauma.

80
Q

What is the Delayed Non-Matching to Sample (DNMS) task?

A

The DNMS task involves a monkey choosing the new non-matching object after a delay to obtain a food reward, testing recognition memory.

81
Q

How do medial temporal lobe lesions affect performance in the DNMS task?

A

Large, bilateral lesions in the medial temporal lobes severely impair performance in the DNMS task, especially with longer delays, indicating the role of the MTL in recognition memory.

82
Q

What causes Korsakoff’s Syndrome, and what are its symptoms?

A
  • Korsakoff’s Syndrome is caused by chronic alcoholism
  • Sypmtoms: Severe memory impairment, confusion, apathy, loss of coordination, and tremors.
83
Q

What areas of the brain are affected by Korsakoff’s Syndrome?

A

Korsakoff’s Syndrome involves lesions in the dorsal thalamus and mammillary bodies.

84
Q

What types of amnesia are associated with Korsakoff’s Syndrome?

A

Both anterograde amnesia (inability to form new memories) and retrograde amnesia (loss of past memories) are associated with Korsakoff’s Syndrome

85
Q

What causes anterograde amnesia in Korsakoff’s Syndrome?

A

Anterograde amnesia in Korsakoff’s Syndrome is caused by lesions in the medial temporal lobe (MTL).

86
Q

What causes retrograde amnesia in Korsakoff’s Syndrome?

A

Retrograde amnesia in Korsakoff’s Syndrome results from cell death in the neocortex.

87
Q

What three types of memory are impaired in Alzheimer’s Disease?

A

Impairs episodic memory, executive function, and semantic memory, though procedural memory can remain intact.

88
Q

What does HM’s ability to perform mirror tracing tasks suggest about memory in Alzheimer’s Disease?

A

HM’s ability to improve on the mirror tracing task despite memory loss suggests that procedural memory is spared in Alzheimer’s Disease.

88
Q

Where are the first signs of Alzheimer’s Disease noticed, and what happens to the affected regions?

A
  • The first signs of Alzheimer’s Disease are noticed in the entorhinal cortex, then proceed to the hippocampus.
    -As the disease progresses, the affected regions begin to shrink as nerve cells die.
89
Q

What are the key pathological features of Alzheimer’s Disease? What does this lead to?

A

Associated with the accumulation of neurofibrillary tangles and amyloid plaques, leading to brain tissue atrophy in areas responsible for memory and language.

89
Q

How do symptoms of Alzheimer’s Disease progress from mild to moderate stages?

A

Mild symptoms include memory loss, confusion, and mood changes. As it progresses, moderate symptoms include difficulty recognizing people, language problems, and increased confusion.

Neurobiology -BIOL4370 (5 decks)

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