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PSYC325 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

what is an egocentric spatial frame?

A

when objects are framed in relation to the self (“I”)
- always carry first person perspective (left-right, up-down, ahead-behind)

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2
Q

what are the 3 egocentric layers of space that the mind distinguishes between?

A
  • personal: within one’s body
  • peripersonal: within reach
  • extrapersonal: beyond reach
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3
Q

what is an allocentric spatial frame?

A

when object (including self) positions are framed in relation to external objects

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4
Q

what are the 2 types of allocentric spatial frames?

A
  • absolute: unchanging (NESW)
  • intrinsic: depends on orientation of reference object (in front of, under, in, on, etc.)
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5
Q

in what way is allocentric better than egocentric?

A

more important for navigating through spatial environments in which we must understand how objects and landmarks are related to each other (where objects are placed relative to other objects)

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6
Q

define wayfinding techniques.

A

distinct cognitive processes for target localization (anything you are doing to get you from one place to another)

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7
Q

what are the wayfinding techniques?

A

reference frames
- egocentric (personal, peripersonal, extrapersonal)
- allocentric (absolute, intrinsic)
relational techniques
- categorical
- coordinate

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8
Q

what are categorical relational techniques?

A

qualitative or nominal relationships (ex. above/below, in, on)
- affect (emotional) valence biases object spatial memory (good-up; bad-down)

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9
Q

where are categorical relational techniques lateralized?

A

left hemisphere
- not language-based -> aphasics do not necessarily show deficits for categorical spatial representations
- left parietal lesion patients make more categorical errors

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10
Q

what are coordinate relational techniques? where are they lateralized?

A

quantitative or metric relationships (4.67m, 42°N, 84°W, three times as far, etc.); lateralized to right hemisphere
- posterior parietal cortex (PPC)
- right parietal lesion patients make more coordinate errors

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11
Q

what are some ways in which aspects of spatial representation are processed in the brain?

A
  • functional cell types (place, grid, time)
  • hippocampal indexes
  • dorsal stream
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12
Q

what are place cells?

A

receive input from many grid cells and code for specific places (fire at specific places)
- located in the dentate gyrus

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13
Q

what are grid cells?

A

receive multimodal input and respond to distinct spatial frequencies (fire at specific intervals to create a grid-like cognitive map of an environment)
- located in entorhinal cortex

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14
Q

what are time cells?

A

sensitive to intervals between key events
- keep track of distances since an important event (ex. Anticipating the end of a lecture at the beginning of it)
- located in the dentate gyrus and entorhinal cortex

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15
Q

what do episodic memories require codes for? where is this information coming from?

A
  • where: position of agent (grid cells)
  • when: sequence of events (time cells)
  • what: content of experience (cells for objects, vectors, emotions, etc.)
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16
Q

how does the hippocampus process spatial representations?

A

hpc is blind to modality, just cares about spatial relationships; general sequence generator for memory (index is a sequence, not a mere reference to a cell assembly)

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17
Q

what is the process of memory formation and recall according to the hippocampal index theory (1)?

A
  • formation: experience is represented in many cortical regions and stored in the hpc by LTP as an index
  • recognition: similar stimuli activate the index, which triggers cortical and subcortical associations of an engram (hpc is a librarian; receives an experience and gives it a code)
  • recall: a sufficient subset of stimuli activate enough of the index to then activate the whole index and engram
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18
Q

what happens when an insufficient subset of info attempts to reactivate an index?

A

memory failure

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19
Q

what is the dorsal stream? what does it include?

A

“where” pathway; supports spatial awareness with 3 output pathways:
- prefrontal pathway (spatial WM)
- premotor pathway
- medial temporal cortex (hippocampal complex; spatial nav, wayfinding)
+ right inferior parietal lobule

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20
Q

what is the premotor pathway responsible for?

A

visually-guided action (plans an action)
- dissociable from purely perceptual or cognitive estimates of distance from visually-guided action (more accurate to reach for an object vs identifying if its within reach)

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21
Q

what is the right inferior parietal lobule (rIPL) responsible for?

A

specialized for tracking distances; specialization for:
- spatial distances
- temporal distances (intervals, time spans)
- social distances (closeness, emotional - ex. how much do you trust someone)

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22
Q

what is an engram?

A

hypothetical construct used to represent the physical processes and changes that constitute a memory in the brain; consciously learned by an individual

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23
Q

what are engram cells?

A

specific neurons that belong to an engram; must follow certain criteria:
1) must be active during learning
2) must be active during memory test
3) when activated they can generate the engram behaviour
4) when inhibited they prevent (or reduce) the engram behaviour

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24
Q

are all neurons active during learning active during retrieval? what experiments illustrate this?

A

no; not all neurons become engram cells
- there is a difference between fear retention based on the training-test interval
- engram cells targeted to die cause the erasure of the conditioned memory

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25
Q

explain this experiment + findings “there is a difference between fear retention based on the training-test interval”

A
  • short intertrial intervals (10s) are remembered much less than longer intertrial intervals (8min)
  • CREB infusion “restores” fear memory trace for 10s intervals (virally infected neurons overexpressing CREB were preferentially recruited to the fear engram)
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26
Q

explain this experiment + findings “engram cells targeted to die cause the erasure of the conditioned memory”

A
  • CREB can be overexpressed by injecting it into neurons
  • CREB overexpression leads to likely selection as an engram cell
  • neurotoxin (diptheria) targets and kills cells that overexpress CREB -> animals that overexpress CREB and treated w/ diptheria fail to remember
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27
Q

how can CREB help a neuron become an engram cell? what competition effect is present?

A

changes the intrinsic excitability of the neuron -> lowers firing threshold, making it more likely to join a Hebbian cell assembly
- CREB-expressing cells will inhibit other cells and prevent them from becoming engram cells -> results in only a subset of cells activated by the learning experience becoming engram cells

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28
Q

what can be used to detect cell activity?

A
  • immediate early genes (IEGs; c-Fos, Arc, ZIF)
  • TetTag mouse
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29
Q

how can IEGs be used to detect cell activity? why is it problematic?

A

expression occurs when a neuron depolarizes, increasing intracellular calcium and activating second-messenger pathways
- genes whose protein products are present after cell activation
- tagged (co-expressed) w/ fluorescent protein to measure
- problem: degrades in mins

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30
Q

what is the TetTag mouse?

A

engineered so Fos promotes the expression of tTA system -> promotes reporter gene LAC (tags recently activated neuron; tells you how much the system has been activated)

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31
Q

what is required to make sure the tTA system is useful?

A

must have temporal control over it
- should promote LAC expression only when the animal is learning
- achieved by the TetTag mouse

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32
Q

what is an experiment using the TetTag mouse?

A

DOX is an antibiotic that blocks LAC expression when consumed
- fear conditioning w/o DOX causes expression of LAC (vs w/ DOX, no expression of LAC)
- LAC and ZIF (IEG) found more often in cells active in animals who froze after fear conditioning -> sign of encoding and retrieval

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33
Q

what are the 2 primary ways of organizing memory types?

A
  • duration
  • dissociable types of stored information in LTM
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34
Q

what are the memory types separated by duration?

A
  • sensory buffer (extremely short) -> info coming in from our senses, running through sensory receptors
  • STM/WM
  • intermediate-term -> memory trace can end here if 2nd wave of protein synthesis doesn’t occur (hrs)
  • long-term
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35
Q

what are the types of LTM?

A
  • declarative: things you know that you can tell others
  • nondeclarative: things you know that you can show by doing; preserved if you have aphasia
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36
Q

what are the types of declarative memory?

A
  • episodic: sequence is important (ex. semantic knowledge doesn’t require knowing the order you learning it); remembering your first day of school (includes autobiographical)
  • semantic: knowing the capital of France
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37
Q

what are the types of non-declarative memory?

A
  • skill learning: knowing how to ride a bike
  • priming: being more likely to use a word you heard recently
  • conditioning (associative learning): salivating when you see a fav food (salivating is an ingram built into the CNS, not learned)
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38
Q

who was H.M.?

A

had debilitating seizures so had a bilateral MTL removal -> could remember some of his past but did not consolidate new episodic memories (anterograde amnesia)
- could develop new skills (ex. Mirror tracing)

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39
Q

what is the unitary view of hippocampal function?

A

all its structures are involved in the production of declarative memories (episodic and semantic memory supported by the same neural system)
- damage to any component of this system will produce the same degree of impairment in tests of episodic and semantic memory

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40
Q

what brain structures does the unitary view of the hippocampus contain?

A

episodic and semantic include:
- parahippocampal ctx
- perirhinal ctx
- entorhinal ctx
- hpc (DG, CA3, CA1), subiculum

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41
Q

what is the modular view of hippocampal function?

A

only episodic memory requires the entire medial temporal hippocampal (MTH) system
- semantic memories can be acquired even when the hpc is selectively removed
- episodic and semantic memory share some components of the MTH system, but overlap is not complete; not part of a single declarative memory systems

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42
Q

what are the modules in the modular view of hippocampal function?

A

episodic memory:
- parahippocampal ctx
- perirhinal ctx
- entorhinal ctx
- hpc (DG, CA3, CA1), subiculum
semantic memory:
- parahippocampal ctx
- perirhinal ctx
- entorhinal ctx

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43
Q

what is the evidence for the modular view of hippocampal function?

A

1) young children w/ MTL damage after ischemic stroke -> no episodic memory
- develop normal language + social skills w/ fully normal levels of vocab and other forms of semantic memory
2) familiarity info does not require episodic content
- rats w/ hpc damage still learn to recognize objects, but do not retain info about learning context

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44
Q

what are the 3 properties of episodic memory?

A

1) supports conscious recollection of contextual spatiotemporal info for later retrieval
- intentional initiation of retrieval
- conscious awareness of remembering
- does not require either to be active
2) it automatically captures episodic and incidental info about single episodes of our lives
- does not require the intention to encode or consolidate memory
3) includes info about the spatial and temporal context that is protected from interference by other memory traces
- the stability-plasticity dilemma: a memory system has to be stable and plastic; we need to be able to remember things and learn new things, need to remain balanced

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45
Q

how does the brain support the properties of episodic memory?

A

through a hierarchy and a loop

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46
Q

what is the hierarchy of episodic memory?

A

episodic experiences are first transduced by sense receptors and then processed hierarchically until they reach the hippocampus (neocortex -> perirhinal + parahippocampal cortices -> entorhinal cortex -> hippocampus)

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47
Q

what parts of the neocortex are involved in the episodic memory hierarchy? what do they do?

A

uni- and polymodal cortical areas
- support perception processes

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48
Q

what are the perirhinal and parahippocampal areas responsible for in the episodic memory hierarchy? what about the entorhinal cortex?

A
  • support associative recall
  • spatiotemporal event context
49
Q

what is the loop of episodic memory?

A

supports sequential indexing of integrated (amodal: hippocampus numb to how info is received/what senses are used) event information

50
Q

what are some characteristics of the loop of episodic memory (role of hpc, etc.)?

A
  • information is most compressed and abstract in hippocampus
  • anterograde amnesia results from damage to hippocampus
  • info goes through loop multiple times (ex. Retrieval runs through hippocampus multiple times to strengthen connections with cortex)
51
Q

what is the hippocampal index theory designed for?

A

to provide an in-principle account of how the neural system in which the hippocampus is embedded can naturally explain episodic memory

52
Q

what aspects of the relationship between memory and the brain does the hippocampal index theory account for?

A

1) the role of the hippocampus in episodic engram formation
2) the nature of the engram
3) the role of the hippocampus in memory retrieval

53
Q

what does the hippocampal index theory say the hpc is for?

A

does not store memories, but rather pointers (indexes) to memories that are stored in the neocortex (engram itself is not in the hippocampus)
- index itself has no episodic memory content; the hippocampus is amodal

54
Q

how does memory formation occur according to the hippocampal index theory?

A
  • memory formation begins when a set of neocortical patterns activated by a particular experience is projected to the hippocampus and activates a unique set of synapses that will become the index
  • the resulting engram consists of those patterns of neocortical activity conjoined by the indexing neurons in the hippocampus
55
Q

how does memory retrieval occur according to the hippocampal index theory?

A

during memory retrieval, when a subset of the initial input pattern activates the hippocampal index, output from the hippocampus projects back to the neocortex to activate the original neocortical pattern

56
Q

how does an index retrieve an episodic memory?

A
  • pattern completion: the ability for the index to restore an entire memory from a single cue
  • pattern separation: a retrieval cue might activate multiple indices, but the most activated one will activate only the engram associated with it
57
Q

what are some pieces of evidence that support the hippocampal index theory?

A
  • context preexposure facilitation: animals that are preexposed to a context are more readily fear conditioned to it -> resulting from pattern completion of the shock from the context cue
  • rats with hippocampal damage will treat explored objects as familiar regardless of context -> failure of pattern separation
58
Q

what are the main areas of research that provide evidence of engrams forming perinatally?

A
  • olfactory
  • auditory (before and after birth)
59
Q

what olfactory evidence shows engrams form perinatally?

A

newborn babies of mothers who ate garlic during pregnancy do not show a typical garlic aversion

60
Q

what auditory evidence before birth shows engrams form perinatally?

A
  • vibrotactile CS and loud noise US used to condition fetus in last 2 months of pregnancy
  • can habituate to loud sounds at 22 weeks
  • respond with head twitches to recordings of fathers’ voice but prefer mothers’ voices
  • cannot discriminate between mother’s recorded voice and another person’s recorded voice at 36 weeks, but can detect mother’s live voice (perhaps not auditory, could be vibrational)
61
Q

what auditory evidence after birth shows engrams form perinatally?

A
  • prefer mothers’ voice over other voices (learn sucking pattern to produce distinct recorded voices
  • discriminate between their native and foreign languages (2 days old; higher frequency sucking when hearing foreign languages)
  • remember melodies presented in 3rd trimester at least 1 month after birth
62
Q

what is childhood (infantile) amnesia?

A

most people have very few “memories” before age 4 (Freud)
- autobiographical memories

63
Q

does childhood amnesia occur cross-culturally? how does it differ?

A

yes
- “West” (US): event-centred with emphasis on entertainment
- “East” (China): socially-centred with emphasis on moral narrative

64
Q

what 2 complementary process account for childhood amnesia?

A
  • vulnerability for early memories (weaker, more likely to get modified/lost)
  • inaccessibility of early memories (partly due to cognitive modularity development)
65
Q

why is it thought that childhood amnesia is due to vulnerability?

A
  • young children do not form and/or consolidate memories like adults
  • the strength of memory formation increases with age
  • possibly due to hippocampus not being mature enough
66
Q

why is it thought that childhood amnesia is due to the hpc not being mature enough?

A
  • episodic memory stabilizes at age 7-8 where it reaches that of adults
  • neurogenesis decreases in early childhood
  • hippocampal-cortical connectivity shoes increases from childhood to adulthood
  • hippocampal volume shows an overall inverted-U shape over development (increases during childhood, begins to decrease in adolescence)
67
Q

what are the region-specific volume changes that occur in the hpc over development?

A
  • adults have smaller hippocampal head (adjacent to amygdala), larger hippocampal bodies, and smaller hippocampal tails
  • CA3-DG and EC decrease in childhood
  • CA1-2 subfields decrease with aging
68
Q

why is it thought that childhood amnesia is due to inaccessibility?

A
  • young children form and consolidate memories, but retrieval is blocked (children can tell stories and fill in gaps in their memories)
  • possibly due to differences in episodic modularity over development
69
Q

what differences in episodic modularity are present over development?

A
  • overall brain weight increase
  • language-specific modularity for simple narrative matures by ages 3-4
70
Q

how is language-specific modularity relevant in episodic memory?

A
  • episodic memory relies on language to understand and generate simple narrative
  • episodic memory retrieval relies on narrative cues for sequence pattern completion (telling a story in the correct order of events)
71
Q

what are the 2 types of consolidation?

A
  • systems consolidation
  • cellular consolidation
72
Q

what is systems consolidation? what does it include?

A

involves the bidirectional interaction between the hippocampal complex and entire network memory trace representation; occurs over days to years
- standard model of systems consolidation

73
Q

what is the standard model of systems consolidation?

A

experience initially lays down a memory trace that depends, for both storage and retrieval, on interactions between the neocortical areas and the MTH system (based on Ribot’s Law)

74
Q

what is Ribot’s Law?

A

older memories are more stable than new memories because:
- the experience is more likely to be repeated
- older memories are more likely to have been recalled and reconsolidated several times
- older memories have survived longer

75
Q

what are characteristics of the standard model of systems consolidation?

A
  • an initial memory trace is a set of weakly connected cortical representations
  • retrieval initially requires the hippocampus’ connections
  • as memories age, the cortical strengths intrinsically increase (systems consolidation) -> retrieval no longer depends on the MTH system since consolidation in the neocortex has occurred
76
Q

what 2 assumptions is the standard model of systems consolidation built on?

A
  • the hippocampal complex is necessary for a limited time after memory trace formation (early memory disruption results from deficits of the hippocampus)
  • the interaction between the hippocampal complex and cortex is only necessary for declarative memories (procedural memories are not affected by hippocampal damage
77
Q

what is cellular consolidation?

A

the biochemical and molecular events that take place immediately following the behavioural experience that initially forms the memory trace, including the strengthening of synapses through processes like LTP; occurs within hours

78
Q

what is senile memory loss?

A

some cognitive abilities worsen with age (WM, LTM, etc.) and some improve with age (vocabulary)

79
Q

how is senile memory loss compensated for?

A
  • there is compensatory activation of the PFC in both hemisphere in elderly subjects with good recall
  • suggests that people who maintain overall cognitive functioning as they age may benefit from brain capacities of resilience or reserve, enabling them to sustain cognitive function despite the aging process (remaining active helps cognition)
80
Q

what evidence is there against normative aging?

A

there are multiple neurodegenerative and cerebrovascular conditions in old age that are associated with cognitive impairment, many of which are difficult to identify antemortem
- neuropathology markers
- vascular dementia
- lewy body dementia
- frontotemporal dementias
- Alzheimer’s dementia

81
Q

how do neuropathology markers show evidence against normative aging?

A

show decrease in global cognition in those with increased AD prevalence, increased cortical Lewy bodies, and increased hippocampal sclerosis
- most cognitive loss is attributable to non-normative processes related to brain pathology or mortality

82
Q

what is vascular dementia? what is it caused by?

A

most severe form of vascular cognitive impairment (ministrokes)
- second most common type of dementia (~15%); increased likelihood as we age due to deterioration of vascular system
- caused by many distinct vascular factors (cardiac arrest, arterial occlusion, hemorrhage, white matter lesions)
- leads to severe cognition deficits, including memory formation and retrieval

83
Q

what is Lewy body dementia?

A
  • loss of tegmental DA neurons and forebrain cholinergic neurons (supply entire cortex with ACh; sharpen/amplify signals to cortex, cancelling out noise)
  • characterized by deposits of a-synuclein in Lewy bodies
84
Q

what are frontotemporal dementias?

A

cluster of degenerative dementias related to deterioration of the frontal and temporal lobes
- behaviour variant (frontal lobe)
- primary progressive aphasias (language regions are reduced)

85
Q

what is Alzheimer’s disease? what is it caused by? what does it lead to?

A

most common cause of dementia (~70%)
- AB plaques: extracellular deposits of insoluble beta-amyloid
- tau tangle: intraneuronal accumulation of abnormally hyperphosphorylated tau
- fatty droplet accumulation
- neurodegeneration
- severe episodic memory loss
- increased vulnerability to interference and false confidence (due to false memory)

86
Q

what are some risk factors for AD?

A
  • APOE4 gene
  • hearing loss
  • social isolation
  • insufficient sleep
  • advanced age
87
Q

what is slow-wave sleep (SWS)?

A

delta waves generated in the cortex that occur in stage N3 of the sleep cycle

88
Q

what are some effects of SWS?

A
  • SWS amplitude precedes large changes in cerebral blood flow, blood volume, and spinal fluid
  • SWS (N3) linked to glymphatic system (clears out metabolic debris, increasing CSF in response to SWS; enhances synaptic signal: noise ratio (sharper)) through hemodynamic oscillations
  • SWS (N3) is the stage most implicated in memory consolidation
89
Q

how is SWS implicated in memory consolidation?

A
  • slow oscillations arise in the cortex and spread to subcortical areas
  • sleep spindles arise from the thalamus and travel to the cortex
  • stimulate early gene expression and glutamate receptors for LTP
  • ripples arise in the hippocampus
  • associated with offline replay of learned sequences during encoding
  • synchronization of these rhythms is believed to ensure memory replay and transfer of learned sequences from the hippocampus to the cortex
90
Q

how are memories consolidated during sleep?

A

coordination of sleep spindles with hippocampal ripples and neocortical slow waves
- during non-REM sleep, neocortical slow oscillations drive the reactivation of hippocampal memory representations during SWR in the hippocampus together with spindles in the thalamic reticular nucleus
- believed to allow new memories in STM or early LTM to be transferred to LTM

91
Q

what experiments have shown the role of SWS in memory consolidation?

A

experimentally enhancing slow oscillations with tDCS (electrodes induce current in the brain) in humans causes an improvement in memory recall
- more word pairs remembered

92
Q

what kind of ripples improve memory?

A

long-duration ripples
- artificially prolonging SWR improves working memory
- artificially aborting sharp wave ripples decreases performance on learned tasks

93
Q

what can bias which memories are replayed during sleep?

A

stimulus cues presented during SWS
- ex) auditory cues - listening to spanish during SWS after learning it in the day can improve its consolidation

94
Q

what 5 subcortical regions are involved in regulating sleep?

A

brainstem nuclei:
- raphe nuclei
- locus coeruleus (+ subcoeruleus)
- basal forebrain
- pedunculopontine
hypothalamic nuclei:
- ventrolateral preoptic nucleus (VLPO)

95
Q

how does the raphe nuclei regulate sleep?

A

serotonergic
- promotes arousal, wakefulness

96
Q

how do the locus coeruleus and subcoeruleus regulate sleep?

A

noradrenergic
- LC: promotes arousal, wakefulness
- subcoeruleus: inhibits motor neurons, promotes muscle atonia during sleep -> damage to this causes movement during sleep (ex. Sleepwalking)

97
Q

how do the basal forebrain and pedunculopontine regulate sleep?

A
  • basal forebrain: GABAergic; promotes sleepiness, SWS (cue u to feel drowsy)
  • pedunculopontine: cholinergic; promotes REM (PGO waves- thought to promote individual aspects of dreams)
98
Q

how does the ventrolateral preoptic nucleus (VLPO) regulate sleep?

A

activation induces sleep

99
Q

what are orexin neurons? what happens when they fail? where are their peptides produced? what do they do?

A

produce arousal (failure of orexin neurons cause narcolepsy)
- orexin peptides are produced by neurons in the lateral hypothalamus
- projections of orexin neurons connect to other areas of the hypothalamus (ex. tubermammillary nucleus and brainstem (LC))

100
Q

how can orexin be a target for sleep medications?

A
  • dual orexin receptor antagonists (DORAs) are developed as sleep-promoting medications (preventing arousal)
101
Q

what kind of waves are present during waking?

A

theta, beta, gamma

102
Q

what is stage N1 sleep? what kind of waves are present?

A

light sleep, alpha waves + occasional vertex spikes
- brain waves begin to slow down from wakefulness
- lasts from 1-7 min
- no significant effects on memory or cognition

103
Q

what is stage N2 sleep? what kind of waves are present? at what frequency?

A

theta, sleep spindles generated in thalamus
- 12-15 Hz
- hippocampal SWRs begin to appear due to synchronization of CA1 interneurons

104
Q

what are sleep spindles implicated in?

A
  • behavioural evidence suggests that sleep spindles are associated with sleep-dependent cognitive and motor performance
  • physiologically, spindles have been shown to support plasticity -> sleep deprivation suppresses neurogenesis in the hippocampus (reduced consolidation of new declarative memories)
  • sleep spindles increase after motor sequence learning -> motor skill learning correlates positively with the amount of stage N2 sleep, when sleep spindles reach peak density
105
Q

how is stage N2 sleep different in schizophrenia?

A

fewer sleep spindles and no sleep-associated motor sequence improvement

106
Q

what is stage N3 sleep? what waves are present? at what frequency? what cognitive aspects does it entail?

A

delta waves; 1-4 Hz, generated by cortex
- contains hippocampal sharp-wave ripples (SWR; 200 Hz), created by broad excitation of CA1 neurons by CA3 pyramidal cells via Schaffer collaterals
- play a causal role in memory consolidation along with slow waves

107
Q

what experiment describes what happens during SWS?

A
  • when rats explore a novel space (maze), place cells are trained to be activated in a specific sequences
  • while awake, place cells fire in reversed order sequence
  • during SWS, place cells fire in sequence at 20x the rate (we replay motor sequences in our sleep)
108
Q

what is REM sleep? what waves are present? at what frequency? what cognitive aspects are occurring?

A

schema disintegration, dreaming
- theta, beta waves, 7 Hz
- involves associative thinking, in which pieces of information are combined in novel ways (I.e. creativity)
- parts of schemas functionally disassembled and reassembled in novel and creative ways

109
Q

what have studies about REM sleep shown?

A

in multiple studies of creative problem solving (ex. Coming up with more novel solutions to problems), associative thinking benefits after being awakened from only REM sleep

110
Q

what occurs when distinct memories are consolidated? how is this represented in the brain?

A

abstracted regularities (patterns) are extracted
- the schema of “dog” can be formed by extracting regularities from instances of poodle, retriever, and hound
- distinct memory instances of dogs have overlapping cortical representations

111
Q

how does SWS help with schema formation and integration?

A

during SWS, the common parts of each cortical representation of dogs are reactivated and reinforced as a generalized schema for “dog”, followed by synaptic downscaling to remove features not fully common

112
Q

how is integrating new memories easier when related schemas are available?

A
  • when a new memory shares features with one or more established schemas, it is more easily appended through reactivation of the schema and Hebbian synapse strengthening
  • synaptic downscaling makes memory-to-schema activation more likely than schema-to-memory reactivation
  • additional memories are similarly appended, which occasionally cause and update to the schema
113
Q

what drugs impair memory?

A
  • alcohol (+ benzos): partial NMDA antagonists, prevent LTP
  • dissociatives: NMDAR antagonists
  • cannabis
114
Q

how does cannabis impair memory?

A

CB1 receptors = memory impairment; decreases theta waves in frontal lobe (thought to entrain cortical areas w/ thalamus; corticothalamic integration); impairs attention + WM capacity

115
Q

what drugs enhance memory?

A
  • stimulants: DA agonists (cocaine, amph), cholinergic agonists (nicotine)
  • nootropics: piracetam taken w/ acetyl-CoA (positive allosteric modulators of AMPARs, enhanced WM, attention, problem-solving, etc.)
116
Q

how is epinephrine related to memory?

A
  • nverted-U relationship between arousal and performance in all aspects of learning and memory tasks (optimal for memory consolidation is ~1 min after learning task, ~1500 pg/ml)
  • general vigilance, time-dependent effects
117
Q

how is cortisol related to memory?

A
  • abnormal high/low levels of glucocorticoids decrease size of DG
  • stress (high cortisol) inhibits neurogenesis in hpc
  • acute stress (moderate cortisol) improves consolidation, chronic stress (high cortisol) impairs memory
118
Q

what are the 2 proposed modules of WM that do not interfere and are controlled by a central executive?

A

in PFC; focus + divide attention, task switching, interface w/ LTM
- phonological loop: rehearsal of verbal items, especially in sequences
- visuospatial sketchpad: rehearsal of object location (sequence) info

119
Q

what is an episodic buffer?

A

involved in WM
- introduced as a way to hold
multidimensional code chunks
- linking perception, WM, & LTM

PSYC325 (2 decks)

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