Chapter 17: Learning and Memory Flashcards

1
Q

Plasticity

A

“changeability” of neurons, mechanisms underlying learning and memory

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2
Q

Learning and memory have only ever been….

A

inferred

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3
Q

Memory is not….

A

instantly formed

(can’t remember something from a moment ago but can remember things from years ago)

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4
Q

Stages of Memory

A

Responsible for our ability to recall things depending on the length of time from event and the mechanisms underlying them.

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5
Q

What are the 5 Stages of memory

A
  1. Starts as senses
  2. Sensory Buffers
  3. Short-term memory
  4. Intermediate- term memory
  5. Long-term memory
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6
Q

What senses are apart of memory?

A

-Visual
-Auditory
-Olfactory
-Tactile

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7
Q

Sensory Buffers

A

An element of the type of memory that stores the sensory impression of a scene

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8
Q

Short-Term Memory

A

A form of memory that usually lasts only for seconds, or if rehearsal continues, especially while being used during performance of a task

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9
Q

What part of the brain does short-term memory involve?

A

Prefrontal cortex
- Each region has different attributes

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10
Q

Working Memory

A

Type of short-term memory that holds a limited amount of information available for ready access during performance of a task (less than 30 seconds)

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11
Q

What is the model of memory?

A

Phonological Loop&raquo_space; Visuospatial sketchpad&raquo_space;
Episodic buffer

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12
Q

Intermediate Term Memory

A

A form of memory that lasts longer than short term memory but not as long as long-term memory

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13
Q

Long Term Memory

A

Enduring form of memory that lasts days, weeks, months or years and has a very large capacity

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14
Q

Encoding

A

Stage of memory formation in which the information entering sensory channels is passed into short-term memory

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15
Q

Consolidation

A

Stage of memory formation in which information in short-term or intermediate-term memory is transferred to long-term memory

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16
Q

What is consolidation resistant to?

A

Disruption and forgetting

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17
Q

Retrieval

A

Process in memory during which a stored memory is used by an organism .

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18
Q

Storage

A

Putting memories away for later use

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19
Q

Rehearsal

A

Simply going over information multiple times

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20
Q

What two factors can help influence long-term memory storage?

A
  1. Connecting new information with old information
  2. Emotional arousal.
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21
Q

Explain the process of memory consolidation.

A
  1. The peripheral stress hormones and amygdala are activated
  2. The amygdala sends axons to various brain structures to influence how those regions process information (can strengthen regions)
  3. Stress hormones can activate the amygdala, and cortisol can directly affect a region

= enhance memory consolidation after learning event

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22
Q

Explain the Patient H.M case.

A
  • Received a bilateral medial temporal lobectomy
  • After the surgery he suffered from anterograde amnesia.
  • He completed mirror tracing and continuously improved his sills but could not recall doing the task
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23
Q

What does the patient H.M. case suggest?

A

Memories are monolithic (there are different kinds of memories)

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24
Q

Bilateral Medial Temporal Lobectomy

A

Removal of hippocampus, amygdala, and cortices around the hippocampus

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25
Anterograde Amnesia
Inability to form new memories beginning with the onset of a disorder, but could remember memories from before surgery
26
What does anterograde amnesia tell us about?
Consolidation vs storage
27
What was patient H.S.'s long term memory affected by?
Anterograde amnesia
28
Declarative Memory
Memories that you can explain with others
29
What was Patient H.M's relation to declarative memories?
He was unable to form declarative memories
30
What are declarative memories broken down into?
1. Episodic memory 2. Semantic memory
31
Episodic memory
Personal memories of life events
32
Semantic memory
General knowledge of the world
33
What parts of the brain do episodic and semantic memory involve?
- Medial temporal lobe - Neocortex
34
Non-declarative Memory
Things you know that you can show by doing
35
What was Patient H.M.'s relation to non-declarative memory?
He was capable of these memories as shown by his skill of mirror tracing
36
What is non-declarative memory broken down into?
- Learning - Priming - Conditioning
37
Skill Learning
Learning to perform a task that requires motor coordination
38
What parts of the brain does skill learning involve?
- Striatum - Motor cortex - Cerebellum
39
Priming
Exposure to a stimulus facilitates subsequent response to the same or similar stimulus
40
What part of the brain does priming include?
Neocortex
41
What is an example of priming?
Being more likely to use a word you heard recently
42
Conditioning
Neutral stimulus acquires the power to elicit the response normally elicited by another stimulus after the two stimuli are paired
43
What part of the brain does conditioning involve?
- Amygdala - Cerebellum
44
What is an example of conditioning?
Salivating when you see your favorite food
45
What are the two kinds of long-term memory?
1. Declarative Memory 2. Non-declarative memory
46
Non associative Learning
A form of learning when an animal/person changes their response to a stimulus without associating it with a positive or negative reinforcement.
47
What is an example of non-associative learning?
Being unaware of an air conditioner that is constantly running
48
Spatial Memory
The ability to remember the location of objects and the spatial relationships between them
49
What part of the brain does spatial memory involve?
- Hippocampus - Cortex
50
What is an example of spatial memory?
Remembering where you put certain objects
51
Explain the Patient N.A. case.
- Patient had damage to the diencephalon, thalamus, and hypothalamus connections - Had similar symptoms to patient H.M (even though N.A doesn't have a damaged hippocampus)
52
What does the Patient N.A. case suggest?
parts of the diencephalon and hippocampus work together in formation of new memories
53
Korsakoff's Syndrome
Failure to recall past events and recognize familiar objects
54
What causes Korsakoff’s Syndrome?
Thiamine deficiency
55
What does thiamine deficiency typically result from?
Alcoholism
56
What parts of the brain are damaged in Korsakoff’s Syndrome?
- Mammillary bodies - Basal frontal cortex
57
Are patients aware when they have Korsakoff’s Syndrome?
They usually deny anything is wrong and confabulate
58
Confabulate
Fill a gap in memory with falsification
59
What does Korsakoff's Syndrome show the importance of?
The medial thalamus and mammillary bodies to form declarative memories
60
Mammillary Bodies
May be important system connecting medial temporal regions to the thalamus
61
Explain the Patient K.C. case.
- Patient sustained damage to the cortex - Could not retrieve personal memories but had good general knowledge
62
What does the Patient K.C. case suggest?
We can subdivide declarative memories into episodic and semantic memories
63
What is the path for how declarative memories are stored and formed?
1. Sensory processing in cortex 2. Parahippocampal, entorhinal, perihinal cortex 3. Hippocampus 4. Medial diencephalon (mammillary bodies) 5. Storage in cortex (layer 1)
64
Primary vs Recency Effect
Tells us we have different TEMPORAL stages of memory
65
What types of effects does hippocampal damage have?
Differential effects
66
Differential Effects
Tells us different neural structures mediate primary vs recency effects
67
FMRI
Used to look at activity during learning, and then look at how well people do during a test a week later - also look at activity during retrieval
68
What does evidence suggest the hippocampal system and prefrontal cortex are important for?
Consolidation and retrieval
69
What is the theory regarding the hippocampus?
The hippocampus slowly puts memories into the cortex, which helps them coordinate overtime
70
Where are memories stored?
Parts of the cortex near the specific sensory cortex involved in the memory.
71
Where does the neocortex store memories?
In different areas for different types of memories
72
Tools vs Animals
Different lesions can produce different loses of memories
73
Place Learning
Learning to orient yourself in an environment and go to the location
74
What part of the brain does place learning involve?
Hippocampus
75
Habitat Learning
Learning to make the same motor response (habits)
76
What part of the brain does habitat learning involve?
Caudate nucleus
77
What is an example of habitat learning?
Always turning right
78
What do rats form?
A cognitive map
79
Cognitive Map
Understanding of the spatial organization
80
What is the key structure involved in the cognitive map?
Hippocampus
81
Hippocampus
Organizes relationships among lots of information, including space and time
82
Explain the different cells in the hippocampus.
-Has spatial cells and place cells - Grid cells feed in to form place cells - The cells for basis for declarative memory formation
83
What are the 3 factors that induce synaptic changes?
1. Environment enrichment 2. Aplysia and simple learning 3. Hippocampus and long-term potentiation
84
What causes memories to be stored?
Changes in the brain
85
Neuroplasticity
The ability of neurons and neural circuits to be remodeled by events
86
How can neuroplasticity be seen?
By electrically stimulating cells and recording post synaptic potentials
87
Long-term potentiation
Repeated fast stimulation of the presynaptic cell can lead to a long-lasting increase in the post synaptic response
88
What are the 3 factors that can store memories?
1. Changes involving synaptic transmitters =Greater release of NT molecules and more sensitive post synaptic membrane 2. Modulation by interneurons = Hyper polarization or depolarization of axon terminals (NT release) 3. Formation of new synapses or rearrangement of current ones
89
What allows ions to pass through the receptor-channel?
Change in the receptor sensitivity or alteration
90
Environmental Enrichment Experiments
Animals are housed in large social groups in special cages containing toys and other features. This condition provides enhanced opportunities for learning perceptual, motor skills, and social learning.
91
What happens to the cortex of animals who undergo environmental enrichment experiments?
They have a heavier and thicker cortex - Cortical neurons have more branches - Larger and more cortical synapses
92
What do environmental enrichment experiments suggest?
The environment dramatically alters the basic physiology and structure of the brain
93
Aplysia
Sea slugs
94
What do sea slugs show?
Habituation and sensitization of reflexes (simple learning and memory)
95
Habituation
Organism becomes less responsive following repeated presentations of a stimulus
96
Sensitization
Organism becomes more responsive to most stimuli after being exposed to unusually strong/painful stimulation
97
What is an example of habituation and sensitization in sea slugs?
Siphon- Withdrawal Reflex
98
Siphon-Withdrawal Reflex
Touch the siphon of a sea slug and it will retract its gill, but will repeat stimulation, it will retract its gill less because it learns there is no danger.
99
What is the siphon-withdrawl reflex causes by?
Changes in the synapse between the sensory cell that detects the touch and the motor neuron that retracts the gill
100
Explain short-term habituation in sea slugs.
- When the sea slug is first stimulated, it retracts its gill to protect it. - If it is stimulated repeatedly, it habituates to the stimulus and no longer retracts its gill. = release less NT
101
Explain long-term habituation in sea slugs.
- When the sea slug is stimulated repeatedly over days, it habituates faster each day. - Eventually the sea slug has no response to the stimulation due to retraction of some synaptic terminals.
102
What can reflexes do?
Sensitize (become more responsive)
103
What is sensitization mediated by?
A facilitating neuron that releases serotonin on the presynaptic neuron.
104
What does the stimulation of presynaptic neurons induce?
Tetanus
105
Tetanus
rapid burst of stimulation
106
What are the 3 pathways where long-term potentiation occurs?
1. Preforant Pathway 2. Mossy Fiber Pathway 3. Schaffer Collaterals
107
Perforant Pathway
Entorhinal cortex >> Dentate gyrus
108
Mossy Fiber Pathway
Dentate gyrus >> CA3 pyramidal cells
109
Schaffer Collaterals
CA3 pyramidal cells >> CA1 pyramidal cells
110
Why is the NMDA receptor voltage gated?
A MG2+ ion blocks the channel unless the cell is already depolarized
111
What would NOT open the NMDA receptor?
A single release of NT
112
Explain the effect of Inducing Long-Term Potentiation
- Rapidly stimulating the presynaptic terminal leads to depolarization and increased NT release. - Activates NMDA receptors which allows calcium to enter the post synaptic neuron. - The influx of calcium triggers intracellular signaling pathways that strengthen synaptic connections
113
Explain the Enhanced Synapse after LTP
- There are more AMPA receptors after LTP occurs = larger postsynaptic response - May have more NT release with a single stimulation
114
Explain the expanded synaptic size after LTP
- After time has passed and new proteins are made, you may get an overall larger synapse with more inside
115
How long do the earlier stages of LTP last?
About an hour
116
What is early stages of LTP dependent on?
1.Change in receptor channel properties - increased conductance makes more sodium come through 2. Change in number of receptors -increased number
117
What is early stages of LTP not dependent on?
Protein synthesis (required for later stages)
118
Correlational Observations
The time course of LTP is similar to the time course of memory formation
119
Somatic Intervention
Things that block LTP and block memory formation
120
Behavioral Intervention
Training in a memory task creates LTP in the brain
121
Where are new neurons produced?
Dentate gyrus
122
What is the production of new neurons crucial for?
Learning
123
What do older adults show deficits in?
-Working memory -Retrieval of memories (requires effort with no external cues)
124
What do external cues help trigger?
memories in older adults
125
What are the 3 causes of deficits?
1. Impairments in encoding and retrieval, less brain activation 2.Loss of neurons/neural connections 3.Deficits in cholinergic transmission (problems in the basal forebrain system)
126