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PSYC325 > Midterm > Flashcards

Midterm Flashcards

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1
Q

what is an ingram? what’s an example?

A

memories that are not learned by an individual in their life
- instinct, built-in adaptations inherited from one’s parents/lineage
- selected when environmental regularities are extremely regular (hyper-stable)
ex) sneezing

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2
Q

what is an engram?

A

memories that are learned by the individual
- require personal experience
- useful when one’s own experience is unique but still relevant to predicting one’s future (quickly changing environment)
ex) learning skills for a new job

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3
Q

what is an example of combining ingrams and engrams?

A

learning a language
- the capacity to learn a language is an ingram
- actually learning the language is an engram

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4
Q

how can you study learning and memory? how did Ebbinghaus contribute to this?

A

learning and memory processes cannot be observed directly, therefore must be inferred by observable behaviour
- Ebbinghaus developed the first scientific methods for assessing the acquisition and retention of a controlled experience

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5
Q

how did Ebbinghaus study “pure memory”?

A

required a methodology that would separate what the subject has learned from what the subject is being asked to remember
- so he invented the nonsense syllable (nuh, vag, boc)
- he was his only subject

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6
Q

what were Ebbinghaus’ research findings?

A
  • test performance increased the more he practiced a given list
  • retention performance was better when he spaced the repetition of a given list rather than when the list was repeated without a break between the learning trials
  • Ebbinghaus’ Forgetting Curve
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7
Q

what does Ebbinghaus’ Forgetting Curve (first forgetting curve) tell us?

A

we forget over time in a non-linear way
- dramatic decrease in % recalled within the first hour, then stabilized but continued to decrease from hrs to days
(most forgetting occurs in the first hr, with progressively less forgetting as time goes on)
- best performance when test was given shortly after learning trial

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8
Q

what did the discovery of the forgetting curve lead to?

A

led to other scientists proposing theories underlying the structure of memory:
- single trace theory
- dual trace theory

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9
Q

what is the single trace theory?

A

the forgetting curve can be explained by assuming that the strength a single memory trace declines monotonically (non-linear) as a function of time between learning and the retention test

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10
Q

what is the dual trace theory?

A

the forgetting curve can be explained as the product of a rapidly acquired short-term trace that has a fast decay rate and a slowly established long-term trace that decays slowly

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11
Q

how did Golgi believe the nervous system was arranged?

A

NS is an exception to the cell theory, being formed not by independent cells but rather by a gigantic net (syncytium) -> continuous reticulum/network
- protoplasmic processes (dendrites) in contact w/ blood vessels and provide nutrients to the cell
- output end of neurons are continuous w/ each other and formed a reticulum

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12
Q

what were Ramon y Cajal’s 2 big ideas?

A
  • neuron doctrine
  • synaptic plasticity hypothesis
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13
Q

what is the neuron doctrine?

A

the idea that the brain is made of discrete cells called nerve cells, each delimited by an external membrane
- refuted the reticulum theory; neurons are truly independent genetically dervied units that are composed of dendrites, soma, and axon
- argued that axon endings were contiguous with dendrites but not continuous with them -> synapse
- basis of modern neuroscience -> neurons are physiological units that pas electrical current in one direction

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14
Q

what is the synaptic plasticity hypothesis?

A

the idea that the strength of a synaptic connection can be modified by experience
- certain experiences can strengthen a synapse, creating memories

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15
Q

what are grid cells? how do they work?

A

neurons located in the entorhinal cortex
- fire at regular intervals as an animal navigates an open area, allowing it to understand its position in space by storing and integrating info about location, distance, direction -> creates a grid/cognitive map
- respond to multiple spatial locations organized in a grid

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16
Q

where do grid cells send information?

A

place cells in the hippocampus
- active when an animal is in different locations, and the combination of activity in many place cells creates an internal map representing a particular environment
- fire at specific locations!

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17
Q

what are Hebbian cell assemblies?

A

diffuse circuits of connected neurons that develop to represent specific percepts or concepts -> structural changes in these make lasting memories possible
- Donald Hebb proposed that modified ensembles of neurons called cell assemblies could provide a substrate for memories

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18
Q

what is Hebb’s saying?

A

neurons that fire together, wire together
- how synaptic connections can be modified
- when an axon of cell A is near enough to excite a cell B and repeatedly/persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cell’s firing B, is increased

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19
Q

how are memories represented at the synaptic level?

A

the changes in connectivity among the collections of neurons responding to a specific experience
- changes are distributed through the neural systems engaged by the memory-producing event
- duration of the changes can be short-lived or relatively permanent, and the content of the memory will be determined by the specific sets of cell assemblies activated by the memory-producing experience

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20
Q

what is the Bliss and Lomo experiment that led to the discovery of LTP?

A

discovered LTP by stimulating (SE) the perforant path and recording (RE) in the dentate gyrus in the hpc of living rabbits

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21
Q

what was the method of Bliss and Lomo’s experiment?

A
  • test stimulus: first applied a weak stimulus (WS) to the perforant path and measured synaptic activity
  • then applied a strong stimulus (SS) to the perforant path
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22
Q

why is it important to start with a test stimulus?

A
  • establishes a baseline
  • helps determine if the inducing stimulus produced LTP, resulting in the test stimulus producing a larger response
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23
Q

what were the results of Bliss and Lomo’s experiment?

A

the SS produced an enduring increase in the synaptic response to the WS -> enhanced response = LTP
- SS potentiated the response to the WS and this potentiation lasted a relatively long time (several hrs)

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24
Q

what is the most common procedure for studying LTP?

A

in vitro preparation:
- places slices of hippocampal tissue in a recording chamber
- used to study LTP induced neurons in the CA1 region of the hpc
- done by stimulating the Schaffer collateral fibres and record field potentials from a RE placed in the CA1 region

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25
what is the hippocampus? what does its pathology include? what are its structural correlates?
cortical structure responsible for memory consolidation - pathology includes anterograde amnesia (inability to form new memories) - part of the hippocampal formation, which includes the dentate gyrus, hippocampus, and subiculum
26
what is the trisynaptic organization of the hippocampus?
important in memory formation and LTP: - neurons in the entorhinal cortex connect to the dentate gyrus (perforant path) - neurons in the dentate gyrus connect to the CA3 region (mossy fibres) - neurons in CA3 connect to neurons in the CA1 region (Schaffer collaterals)
27
where is the hippocampus? why is does this make it an important brain structure?
hpc is part of the medial temporal lobe system, where it is the central structure and works with adjacent regions (entorhinal ctx, perirhinal ctx, parahippocampal corticies) - responsible for governing long-term memories - acquiring new memories is a distinct, separable process from other cognitive abilities such as perception
28
where does LTP occur?
hpc -> suspected mechanism for memory formation - synapses are fundamental units of storage in the brain - Schaffer collaterals in hpc are most studied site of LTP
29
who has patient H.M.? how does this make the hpc an important structure?
had memory deficits, including anterograde amnesia (STM intact, LTM deficient) - had bilateral MTL removal, which includes hpc
30
why is the hippocampus thought to be an important brain structure for memory?
- part of MTL - LTP - patient H.M.
31
what are the 3 dimensions of memory traces?
- duration (how long a memory lasts; divided into short-term and long-term) - state - vulnerability to disruption
32
what does "state" mean as a dimension of memory traces?
whether the memory is in an active or inactive state - active state associated with STM, more prone to disruption - inactive state associated with LTM, more resilient to disruption
33
what does "vulnerability to disruption" mean as a dimension of memory traces?
how susceptible the memory is to being lost or disrupted - active, short-term memories are more vulnerable to disruption (rapid decay) vs inactive, long-term memories that are less vulnerable (slow decay)
34
what experiment explains how active traces are more prone to disruption? what were the results?
football player has 2 sets of experiences: E1 (before game) and E2 (just prior to head trauma) - E1 memories are older than E2 memories; trauma produces amnesia for only E2 memories because they are still in an active state when trauma occurs - E1 memories are not affected b/c they have achieved the inactive, long-term memory state
35
what can be interpreted from the football experiment?
- memories become more resistant to disruption as they age - memories in the active state are more vulnerable to disruption than memories that have become inactive
36
what is the "Levels of Processing" theory for the creation of memory traces?
without encoding - levels refer to levels of perceptual processing depth (not memory encoding) - memory trace is understood as a byproduct of perceptual analysis and that trace persistence is a positive function of the depth to which the stimulus has been analyzed
37
what example factors can increase the depth of retention, according to the LOP theory?
- amount of attention devoted to a stimulus - stimulus compatibility with the analyzing structures - processing time available - motivation - stimulus salience
38
what is the "General Abstract Processing System" theory for the creation of memory traces?
with encoding; understanding episodic memory - act of memory begins with encoding and ends with retrieval - encoding is not the same thing as perceptual analysis (it is another process) - perceptual analysis is necessary but not sufficient for memory trace formation
39
what are the steps of the GAPS theory?
1) encoding: the process that converts an event into an engram (memory trace) -> depends on the perceived event and the cognitive environment 2) ecphory: the process that combines info in the engram and the retrieval cue into ecphoric info 3) ecphoric info: determines recollective experience, and the end product of an act of cognitive memory
40
what is some psychological and physiological evidence that suggests encoding is a separate process from perception?
- interruption of encoding - remembering events that never happened (not perceived; ex. dreams) - anterograde amnesia (perception intact, no memory trace) - psychopharmacology of encoding - EEG - fMRI
41
how does interruption of encoding suggest that encoding is a separate process from perception?
reduced recall for familiar items that precede a high-priority item, but only when items are presented quickly (ex. a list provided that needs to be remembered as well as possible, told to remember a name (high-priority)) - control = no name (no high-priority item) - items preceding high-priority item are remembered less -> not a problem w/ perception b/c control had no problem w/ recall
42
how does psychopharmacology of encoding suggest that encoding is a separate process from perception?
benzodiazepines do not reduce the perception of stimuli, but those stimuli are not recalled as well afterward
43
how does EEG suggest that encoding is a separate process from perception?
Sanquist et al., 1980: first EEG study to show systemic differences in ERPs between words in a list that were subsequently recalled, and words that were not - differences in ERPs were inferred to reflect encoding
44
how does fMRI suggest that encoding is a separate process from perception?
Wagner et al., 1998: first fMRI study to localize encoding of words that were subsequently remembered vs those that were not - found encoding was reflected by more activity in the left prefrontal and temporal cortices (where language is processed) - no evidence of perceptual or other cognitive differences during testing - damage to prefrontal regions associated with memory deficits but not with perceptual deficits
45
what is the structure of NMDA receptors?
4 subunits - all functional NMDA receptors contain GluN1 subunits - there are multiple GluN2 subunits - composed of GluN1-GluN2A and GluN1-GluN2B subunits
46
what happens when there is GluN1 deletion in CA1?
LTP could be induced in the dentate gyrus but could not be induced in the CA1 region - the mice were impaired on the hidden platform version of the Morris water escape task
47
what happens when there is GluN2B expression limitation?
could impair an animal's ability to learn and remember
48
what happens when there is GluN2B overexpression (Doogie mouse)?
Doogie mouse: GluN1-GluN2B NMDA complex is overexpressed in cortex, amygdala, hpc, etc. - slices show enhanced LTP - shows a stable and enhanced memory for a contextual fear-conditioning experience
49
what is APV?
NMDA receptor antagonist
50
what are ampakines?
positive allosteric modulator on AMPA receptor -> when bound with glu, keeps channel open for longer - enhance learning
51
what is required for exocytosis of AMPARs?
CaMKII
52
what experiment did Malinow conduct to study AMPA receptor trafficking?
genetically engineered GluA1 subunits that had electrical conductance properties that were different from endogenous GluA1s
53
what method was used to study AMPA receptor trafficking by Malinow?
- labeled GluA1 receptors w/ fluorescent proteins - used a viral vector system to deliver these receptors into neurons in amygdala - inserted modified glu receptors (GluA1) into lateral amygdala - exposed the mice to a fear conditioning experience (tested for fear of a tone paired w/ shock or fear of a tone unpaired w/ shock -> rats in paired condition displayed fear of tone)
54
what were the results of Malinow's experiment studying AMPA receptor trafficking?
- fear conditioning had driven GluA1 AMPARs into spines - after training, rats in the paired condition had more GluA1 AMPARs trafficked into PM of spines than rats in unpaired condition **indicate that a behavioural experience that produces fear conditioning also drives AMPARs into synapse**
55
what follow-up experiment was conducted using dummy AMPARs?
modified non-functional GluA1 receptors and injected them into lateral amygdala -> compete w/ endogenous functional GluA1 receptors for trafficking into spines
56
what were the results of the follow-up experiment using dummy AMPARs?
rats injected w/ modified receptor displayed impaired fear conditioning to a tone paired w/ a shock - slices from animals injected w/ modified receptor cannot sustain LTP induced in lateral amygdala
57
what is anisomycin (Anis)? what are its effects?
inhibitor of protein synthesis; when infused into the hpc of rats: - before training has no effect on STM, but disrupts LTM traces - immediately after training, allows for weak LTM traces, decays quickly - 1 day after training, stronger LTM trace produced but also decays - 2 days after training - stable LTM **therefore, takes ~2 days for rats to consolidate a memory**
58
what is Rapamycin?
blocks mTOR
59
what is 4E-BP2? how does mTOR affect it?
usually prevents transcription - mTOR phosphorylates it, removing its inhibition on transcription
60
according to neurobiologists, when has memory consolidation occurred?
when the memory is no longer vulnerable to pharmacological treatments that interfere w/ protein synthesis initiated by learning events
61
what is the first wave of protein synthesis involved in memory consolidation?
BDNF -> TrkB -> mTOR -> TOP - involves local protein synthesis (mRNA + polyribosomal complexes in dendritic spines)
62
how does the first wave of protein synthesis begin?
synaptic activity stimulates brain-derived neurotrophic factor (BDNF), which increases protein synthesis by binding the TrkB receptor
63
what happens when BDNF binds the TrkB receptor?
activation of the mTOR complex
64
what is the structure of the mTOR complex?
dimer: - mTORC1: sensitive to rapamycin; increases local protein synthesis - mTORC2: insensitive to rapamycin, but mTORC2 KO animals have LTM deficits
65
why do mTORC2 KO animals have deficits in LTM?
- mTORC2 promotes polymerization of actin - actin forms the cellular cytoskeleton, and therefore helps determine the shape and size of dendritic spines
66
what happens when the mTOR complex is activated?
mTOR complex phosphorylates the translational repressor protein 4E-BP2 to allow the assembly of functional ribosomal complexes and the rapid translation of TOP mRNAs - translation of TOP mRNAs increases the number of polyribosomes, allowing proteins for synaptic growth to be synthesized at a faster rate
67
what post translational modifications occur after the first wave of protein synthesis?
- AMPAR trafficking - enlarged actin cytoskeleton
68
what are some possible disruptions of the first wave of protein synthesis?
- rapamycin blocks mTOR - mTORC2 KO animals - TrkB-IgG and K252a inhibit BDNF
69
how does rapamycin disrupt the first wave of protein synthesis?
rapamycin blocks mTOR - when infused in the hpc before training, trace lasts 1 hr (first wave disrupted; second wave also disrupted b/c first wave cannot be completed) - when infused after training, the fear avoidance memory trace is persistent (local protein synthesis is not disrupted, enough time has passed)
70
how do mTORC2 KO animals disrupt the first wave of protein synthesis?
LTM deficits due to decreased polymerization of actin cytoskeleton (post translational modifications cannot occur) - STM lasts less than 4 hrs
71
how do TrkB-IgG and K252a disrupt the first wave of protein synthesis?
inhibit BDNF - if delivered 1 hr after training, reduced retention 1 and 7 days later (first wave disrupted)
72
how many peaks does BDNF have?
2; b/c involved in both waves - 1 hr after training - 12 hrs after training
73
what is the second wave of protein synthesis involved in memory consolidation?
BDNF -> CREB -> C/EBPβ -> BDNF (positive feedback loop) - involved genomic protein synthesis in the nucleus/cell body of the cell
74
how does the second wave of protein synthesis begin?
BDNF initiates genomic signalling that leads to the phosphorylation of cAMP response element-binding protein (CREB)
75
what does CREB do once its phosphorylated?
2 things: - targets transcription of genes for synaptic proteins (SPs) to be transported to the stimulated dendritic spine - targets the transcription of C/EBPβ (begins to be expressed ~9 hrs after CREB increases)
76
what does C/EBPβ do?
promotes the transcription of BDNF (hence the second wave)
77
how long does the positive feedback loop run for?
~48 hrs (i.e. if pathways disrupted after 48 hrs, LTM will remain intact) - creates LTM that lasts > 7 days
78
how can the second wave of protein synthesis be disrupted?
- antisense ODNs - blocking C/EBPβ expression - Trk-IgG and K252a inhibit BDNF
79
how can antisense ODNs disrupt the second wave of protein synthesis?
- injecting these disrupt CREB synthesis - lack of CREB does not interfere w/ STM, but prevents LTM formation
80
how does blocking C/EBPβ expression disrupt the second wave of protein synthesis?
- no second peak of BDNF - inhibiting BDNF inhibits CREB - inhibiting C/EBPβ at 5 hrs post training impairs LTM, but supplying BDNF restores the memory trace
81
how do TrkB-IgG and K252a disrupt the second wave of protein synthesis?
inhibit BDNF - if delivered 9 hrs after training, reduced retention only 7 days later (second wave disrupted) - if only first wave occurs, LTM lasts ~2 days
82
how long do memory traces last after each step of memory consolidation?
- after post-translational modifications, STM lasts less than 4 hrs - after 1st wave, LTM lasts ~2 days - after 2nd wave, LTM lasts > 7 days
83
what is the reconsolidation theory?
1) when a memory is retrieved, the synapses underlying the memory become unbound, weakened - retrieving memories make them vulnerable to disruption 2) retrieval also initiates another round of protein synthesis so that the trace is reconsolidated - the trace is updated and stored again in re-strengthened synapse
84
what is memory trace destabilization?
retrieving a memory itself will unbind or destabilize the synapse that supports the memory
85
what does trace destabilization require?
increase in dendritic spine Ca2+; different sources: - amygdala: NMDA receptors - hippocampus: voltage-dependent Ca2+ channels (vdCCs)
86
how do we know that without Ca2+, there is no trace destabilization?
if NMDARs or vdCCs are antagonized prior to reactivation, the trace does not destabilize and anisomycin has no influence on the reactivated memory trace (b/c synapse does not become strengthened again)
87
what are the 2 effects of Ca2+ influx?
1) scaffolding proteins (which hold AMPARs in place) are tagged for degradation) 2) proteosomes (degrade proteins) translocated from dendritic shaft to dendritic spines
88
what is an example of a scaffolding protein that is degraded during trace destabilization?
Shank = master scaffolding protein - holds other scaffolding proteins together in the post-synaptic density
89
how do we know that proteosomes are active during trace destabilization?
βlac is a proteosome inhibitor - preventing protein synthesis w/ Anis typically degrades reactivated traces - βlac inhibition prevents Anis-induced memory trace degradation (proteosomes inhibited from degrading memory, therefore new proteins aren't being made to be disturbed with)
90
do all memories become destabilized when reactivated?
no; very strong or very old memories are difficult to destabilize (ex. trauma is very hard to forget b/c it is a strong association - memories established using weak training parameters are more easily destabilized
91
what is the prediction error hypothesis?
mismatch; occurs when a retrieved memory does not adequately anticipate current experience - triggers destabilization (requires update of memory)
92
what experiment illustrates the prediction error hypothesis?
- rats trained on a CS-US delay of 30s had destabilized traces after Anis injection followed 10s CS-US delay (could not update memory) - memory was a poor predictor, thus requiring update
93
what experimental evidence is there that destabilization can occur without behavioural expression? what conclusion did they come to?
- CNQX - Ifendopil the engram exists independent of behaviour
94
what did the CNQX experiment entail?
AMPA receptor antagonist CNQX was injected into the rat amygdala 24 hrs after fear conditioning - anisomycin injected after presentation of the fear cue (tone) - fear of memory was still reduced despite blocking Ca2+ influx
95
what did the Ifendopil experiment entail?
NMDA antagonist Ifendopil blocks Ca2+ influx - anisomycin injected after tone - destabilization was prevented

PSYC325 (2 decks)

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