Week 11 RF-Episodic memory updating: Implications for psychopathology risk across the life course Flashcards

1
Q

What is Memory Transience and Forgetting? (Richards & Frankland, 2017)

A
  1. Store a memory
  2. Learn something new (forget old memory to promote flexibility)
  3. Make a prediction (forget particulars to generalise)
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2
Q

Why is Memory Flexibility/Forgetting, adaptive in dynamic environments? (Richards & Frankland, 2017)

A

Is adaptive because it:
* promotes behavioural flexibility by eliminating outdated (and potentially misleading) information and creating “space” for new learning

  • prevents overfitting (one interpretation of something) and fosters generalisation
  • Simple (gist-like) memories are better at predicting new experiences in changing environments
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3
Q

What are contributors to episodic memory flexibility?

A

Flexibility = liability of existing episodic memories to adapt in response to external information from the environment and/or in response to internal neurobiological processes, be they “natural” (maturation/ageing) or treatment
induced

(A)Internally driven
* Neurogenesis (creation of new neurons in the hippocampus contributing to the reorganisation of the neurobiological substrate of memory linked to how the memory is cognitively represented in our minds)

(B) Externally/environmentally driven
* Environmental changes
* Reactivation (e.g., environmentally cued)
* The new environment in which you are retrieving the old emotional episodic memory representation would need to be updated e.g., sense of warmth when thinking about a close family member who has passed away.

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4
Q

What is the life-course of an episodic memory? (Phelps & Hofmann, 2019)

A

-A memory becomes frailer each time it is retrieved

-Right after encoding and each time you are retrieving the memory is when it is most likely able to be changed and thus incorporate new information

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5
Q

Emotional Episodic Memory: What is Editing Consolidation? (Phelps & Hofmann, 2019)

A

-The encoding of a memory is dependent on the release of stress hormones

Study:Stress Hormones
-Looked at those who experienced a traumatic event and gave medication that would lower the stress following the traumatic event

-The subsequent event of the retrieval of the traumatic event was associated with less arousal (blocked the release of stress hormones) BUT the emergence of later PTSD symptoms was not influenced

-The aim of exposure therapies is to try and get rid of the sense of danger associated with that traumatic memory

-Impair/enhance memory

Study: Memory Control
-Provided with a cue and asked not to recall the event

-When memories were reactivated but retrieval was blocked, were less well remembered (Generally used to impair memory)

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6
Q

Emotional Episodic Memory: What is Editing Re-Consolidation? (Phelps & Hofmann, 2019)

A

Study: Pharmacological Blockade
-Generally intended to impair memory

Study: Updating Episodic Memory
-Impairs memory + modifies memory content

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7
Q

What is the association between episodic and emotional memory? (Levy & Schiller, 2021)

A

Emotional Episodic Memory:
-The association and the sense re-experiencing is linked to an emotion e.g., threat + the item evoking that emotion (i.e., danger).

-Life-threatening experiences can create an association between a neutral stimulus (e.g., blue car) and the perception of danger (and this is what interventions attempt to do i.e., shift it from emotional to neutral.

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8
Q

What is the role of Re-activation and Re-consolidation in (Emotional) Episodic Memory? (Levy & Schiller, 2021)

A

Reconsolidation:
* Memory updated, weakened, strengthened, or unchanged + Extinction (extinction does not replace the old memory but instead creates a new one and can create a sense of safety which is stronger to the older one i.e., less likely to be reactivated).

Reactivation:
* Memory accessed from long-term store

Destabilisation:
* Memory in labile state

-Pharmacological/Behavioural interventions inbetween Destabilisation and Reconsolidation have been attempted (i.e., between the stage where a memory is labelled and when it is again ready consolidated).

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9
Q

What is the role of updating in Emotional Episodic Memory? (Lee, Nader, & Schiller, 2017)

A
  • The reminder reminds the individual of the emotional event

3 ways in which memory can be updated:
1. The reminder is presented without the threat (can be enhanced pharmacologically) (i.e., extinction as you’re attempting to create that sense of safety).

  1. The reminder is paired with a rewarding
    stimulus (i.e., comfort conditioning)
  2. The reminder is paired with information that competes with the memory trace for the same processing resources (interference)
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10
Q

What are the Brain Systems involved in Emotional Memory? (Levy & Schiller, 2021)

A

-The amygdala is involved in emotional arousal

-The amygdala, hypothalamus and the hypothalamic pituitary adrenal that is associated with the stress response

-The striatum is involved in devising action plans to deal with any threats

-The hippocampus is a key area involved in switching the focus

-The dorsal anterior cingulate is involved in long-term threat maintenance

-Areas in the prefrontal cortex are responsible for dealing with the threat and regulating emotional reactions

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11
Q

What brain regions are involved in updating for emotional episodic memory? (Silva & Graff, 2023)

A
  • Prefrontal cortico-amygdalar systems particularly relevant for reconsolidation in
    both rodents and humans
  • Prefrontal dampening of hippocampal and amygdalar activity may be key to emotional memory extinction (retrieval stopping, Anderson & Floresco, 2021).
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12
Q

How is the Amygdala involved in Fear Conditioning? (Agren et al., 2012)

A

-Day 1: Participants presented with 2 objects (lamps of different colours one associated with electric shocks another wasn’t)

-Day 2: Reactivation- P’s fitted with electrodes to reinstate the context and broken down into 2 groups: one saw multiple presentations without the shock (to show safety and erase the association between the colour and the shock lasting 10 mins). The second group had seen the association between the lamp and the shock without the shock but after 6 hours the memory was reconsolidated.

-Day 3: P’s were scanned with no shock received whilst viewing images of the lamp paired with the shock and without

-Final day: unpaired shocks then viewed both colours of the lamp without a shock

Results:
-6 hour group and 10 minute group did not differ in terms of acquistion and extinction

-Greater amygdala activation compared to the extinction group indicating that the group that received the extinction outside the window where the intial threat memory could be modified, had a stronger association between the colour that ahd been paired with the shock and the shock itself also showing automatic indicators of greater fear.

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13
Q

Give an example of the Amygdala in Fear Conditioning? Lifelong Spider Phobia (Bjorkstrand et al., 2016)

A

-After P’s had an activation of the critical fear construct (the spider), they were then exposed to safe images of the spider in the lab

-BUT they were exposed to these images either in the 6 hour window (already consolidated) or the 10 minute window (where the association and fear was still liable to change)

-Wanted to see if the activation of the amygdala is from seeing an image of the specific spider shown, or would generalise to any image of a spider.

Findings:
-Greater amygdala activation was seen for those who were exposed outside the reconsolidation i.e., already consolidated (so a greater association between the spider and a greater sense of threat compared to the group who had exposure when the memory was liable to change).

-Also asked about their likelihood of approaching the spider with varying monetary rewards. The higher the reward, the greater change in behaviour with the weaker association between the spider and the fear, compared to the group that was less likely to involve safety in their representation of the spider due to a later exposure (i.e., the 6 hour group).

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14
Q

What is the role of the Dorsolateral Prefrontal Cortex in updating emotional episodic memory? (Su et al., 2021)

A
  • TMS Study
  • Stimulation of the right dlPFC hinders the reconsolidation of recent fear memory.
  • Stimulation of the right dlPFC hinders the
    reconsolidation of recent fear memory within a specific time window.
  • Stimulation of the right dlPFC hinders
    reconsolidation of remote fear memory.
  • Those whose reconsolidation was not interfered with for the threat of memories, showed greater SCRs indicating greater arousal
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15
Q

What is the link between INCOMPLETE REMINDERS AND EPISODIC MEMORY UPDATING (Sinclair & Barense, 2018)

A
  • Created a sense of surprise by cutting out the critical moment in a sports video (i.e., a goal) i.e., an interrupted action-outcome event
  • Both groups saw the full video the first day and then one saw the interrupted or full video the next day. Then following this, there was a break between the consolidation video by showing semantically related videos

*For both the interrupted and full video, the group presented with the semantically distracting videos were more likely to incorporate the interfering information in their memories of the initial video (shows how neutral episodic memory can be interfered with as long as it is in the window where the memory is frail).

  • Prediction error (because of the disrupted sequence)
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16
Q

What is the link between PREDICTION ERRORS AND EPISODIC MEMORY UPDATING (Sinclair et al., 2021)

A

-Both groups immediate or delayed, recall a similar number of correct details which tends to be better when the video is interrupted (associated with a sense of surprise).

-For false memories, incorporating new information from the surrounding experimental context was significantly higher for the group tested on day 3 compared to the immediate response after the reactivation of the videos.

17
Q

What are emotional memories like in PTSD? (Gagne, Dayan & Bishop, 2021)

A
  • Intrusive and vivid recollections of the traumatic event(s), accompanied by nightmares
  • Ruminate on the traumatic episode
  • Frequent replay of the events preceding the traumatic episode
  • Updating/augmenting the initial trauma memory with the distress evoked by its
    retrieval
  • Potential role in maintaining PTSD symptoms
  • Habitual tendency to ruminate may be a risk factor
18
Q

What is the role of Inflexibility in emotional memory for those suffering with PTSD? (Kheirbek et al., 2012)

A

-ONSET: Reduced neurogenesis as a risk factor for developing PTSD following trauma (linked to a reduced ability to differentiate representations of an item presented in different contexts e.g., flowers on the field or vase)

-PTSD: Generalisation stemming from poor pattern separation due to reduced neurogenesis (pre-trauma/direct
consequence of trauma)

-Healthy: Discrimination supported by adequate pattern separation skills

19
Q

What are some Pharmacological Interventions for PTSD? (Levy & Schiller, 2021)

A

Reactivation:
* Memory accessed from long-term store

Destabilisation:
* Memory in labile state
(Noradrenergic beta blocker used in between destabilisation and reconsolidation)

Reconsolidation:
* Memory updated, weakened, strengthened, or unchanged

20
Q

What are some Pharmacological Interventions for PTSD? (Brunet et al., 2018)

A
  1. Pharmacological Blockade
  2. Memory Reactivation
  3. Clinical Outcome

Injected with Noradrenergic beta-blocker (propranolol) –> read 1-page trauma narrative (30 mins) (to create a sense of safety with the event) –> Read the narrative to the experimenter (Repeated weekly for up to 6 weeks) –> PT-D
symptoms (self/clinician-rated)

  • Repeated traumatic memory reactivation (became weaker the sense of danger), preceded by noradrenergic blockade, was
    linked to substantial reduction in PTSD
    symptoms
  • Stripping the traumatic memory of its
    adverse emotional arousal?
21
Q

What are some Cognitive Behavioural Interventions for treating PTSD? (Levy & Schiller, 2021)

A

Script-driven Imagery of Trauma used in between Destabilisation and Reconsolidation

22
Q

What are some Cognitive Behavioural Interventions for treating PTSD? (Vermes et al., 2020)

A

Day 1 (pre-intervention):
-SCR (skin conductance responses) and subjective responses to traumatic imagery

Days 2 & 3 (imaginal exposure sessions):
-5 to 10 mins trauma retrieval then the same but neutral retrieval
-1 hour
-1 hour Imaginal Exposure Session (really traumatic or really neutral)

Day 4 (post-intervention):
-SCR and subjective responses to traumatic imagery

-The intervention impacted physiological (SCR) responses (lower responses), but not subjective experience (VAS)

23
Q

What are some Cognitive Behavioural Interventions for treating PTSD? (Speer et al., 2021) NON-CLINICAL

A

-4 groups: one had to focus on the positive aspects of a negative event, one had to look at the negative aspects, one had to look at the neutral aspects, and one had distractions.

-Those with the positive focus, had a higher level of positive feelings with the initial negative event a week later as well as 2 months after the re-interpretation.

-The change in positive feelings was associated with a change in positive emotional details they could recall from the event.