Emotion and memory

Question 1

What paradigm is associated with the iconic memory and how is it researched in relation to emotion?

Answer 1

The Sperling paradigm is adapted so that the cued partial report presents threatening, positive or neutral targets to remember. Researchers then measure if there is a preference for effect for any particular emotional valence or in general.

Question 2

What has been found through these studies of emotion on the iconic memory? (2/3)

Answer 2

It was found that emotional stimuli capture attention and improve short term memory: across all cue delays higher accuracy for emotional (in particular threatening) stimuli.

Emotion slows decay of the iconic memory: Less performance drop with longer cue delay for threatening stimuli.

No differences in initial availability in iconic memory (no additional emotion boost at shorter cue delays)- but some evidence in replication study.

Main findings were that emotional valence boosts iconic memory and results in a slowed decay.

Question 3

Summarise two emotional effects associated with the attentional blink tasks

Answer 3

Emotional attentional blink: Attentional blink at short temporal lags between two target items, Smaller attentional blink when second item is a negative word. No emotional boost present with bilateral amygdala damage (here, patient S.P.).

Emotion-induced blindness: A to-be-ignored emotional ”T1” (distractor) captures attention, impairs “T2” performance. General idea that emotion may be processed through a fast, effortless, reflexive, implicit, parallel, non-conscious, automatic (“Type 2”) system (Dual-systems theory).

Emotion improves performance when it is task relevant, impairs performance when it is task irrelevant.

Question 4

How may these effects be reflected in someone who is a victim or armed robbery?

Answer 4

Weapon focus effect: Effect of weapons on eyewitness testimony in that generally there is a worse memory for perpetrator or circumstances of crime involving weapons, instead much more focus and recollection on the weapon. Mostly studied in the laboratory but evidence for effect in the real world as well.

Question 5

Give two possible explanations for this weapon focus effect

Answer 5

Partially reflects unexpectedness of the weapon (unusual item) (seeing it at a shooting range vs tennis court). Partially reflects emotion (arousal, threat) that narrows attention.

Question 6

Describe the possible neural mechanisms associated in this emotional modulation of visual processing

Answer 6

Feedback connections between amygdala and visual cortex: The Amygdala lateral nucleus (L) receives input from the ventral visual cortex (also possibly coarse visual information from subcortical pathways). The amygdala then sends connections back from its basal nucleuys (B) to virtually all visual cortical areas (even V1).

Question 7

Where is evidence found that the amygdala is key for this feedback modulation related to emotion?

Answer 7

Studies that look at patients with hippocampus vs amygdala damage. Patients with hippocampus damage show normal fusiform cortex emotional enhancement to fearful vs. neutral faces. Patients with additional amygdala damage show normal fusiform face processing but no emotional enhancement in fusiform cortex to fearful vs. neutral faces. Both participants still show selective activation in the fusiform area for faces vs houses, suggesting that this difference is specific to emotion.

Question 8

Describe the classical view which results in a distinction drawn between implicit emotional conditioning and an explicit episodic memory

Answer 8

The classic view proposed by LeDoux was that emotional conditioning involved the amygdala and resulted from subcortical inputs. It was an emotional memory and highly persistent (can’t be erased.)

Contrasted with this, the episodic memory involved the hippocampus and the MTL, resulted from cortical inputs. It was a contextual memory and emotion simply boosted the memory/ vividness or the confidence.

Question 9

Describe the most influential study giving evidence for this distinction

Answer 9

Demonstrated evidence for a double dissociation between patients with bilateral hippocampus damage and those with bilateral amygdala damage and those with both. Those with bilateral hippocampus damage displayed little declarative memory in a task but showed effects of fear conditioning while those with amygdala damage could remember the details of the task but did not show signs of fear conditioning. Neither were present in patients with damage to both areas.

Question 10

Comment on the acquisition of fear conditioning in the standard model of rodent fear conditioning

Answer 10

Acquisition: Pathways conveying CS (cue) and US (shock) converge in the LA, where they strengthen synaptic responses to the CS

Question 11

Describe two routes in which CS and US information can travel to the amygdala in the standard model of rodent fear conditioning

Answer 11

Pathways conveying CS (cue) and US (shock) converge in the LA, where they strengthen synaptic responses to the CS

1) Subcortical “low road” via thalamus sufficient for fear conditioning (coarse stimulus information)
2) Cortical “high road” via cortex: Detailed stimulus information (e.g. discrimination between two tones), can inhibit output from CE and override the low road course fast processing.

Question 12

How do persistent learning induced changes occur at multiple levels in the standard model of rodent fear conditioning, specifically in the lateral nucleus? (3)

Answer 12

=>At the level of the neuron: Changes in dendritic spines (density, branching) via calcium entry (NMDA receptors and voltage-gated calcium channels) and changes in patterns of connectivity

=>Changes in subset of synapses: changes in synaptic strength (long-term potentiation) and changes in neuronal excitability

=>Changes at the nuclear level: Intracellular changes involving protein kinases, gene transcription factors (e.g. CREB), immediate-early genes (e.g. Fos, activity-regulated cytoskeleton-associated protein), changes in DNA structure (histone modifications and DNA methylation), phosphorylation, trafficking of receptors, etc.

Question 13

A scientist once said “what I cannot create, I do not understand.” How has this almost come to fruition in memory research?

Describe this is stages

Answer 13

Finding the fear engram: Allocate-and-manipulate

Allocation: Transgenic mice have been created where the activity of a small subset of LA neurons is increased (made more excitable) at a time of memory encoding (fear conditioning.) (e.g. via viral expression of CREB or via optogenetics, or, here, via designer receptors DREADD)

Encoding: Neurons active during training are allocated to a fear memory engram in LA

DREADD induced inhibition: Pharmacological silencing of tagged (DREADD) engram LA neurons: Reduced freezing

DREADD induced excitation: Pharmacologcial activation of tagged (DREADD) engram LA neurons: Artificially induced memory retrieval
=>Freezing in a novel context in absence of the tone CS

diagram in docs

Question 14

What can these engram cells be considered as conceptually?

Answer 14

Physical substrate of memory (learning and retrieval)

Question 15

What is the proposed role of the hippocampus in fear conditioning?

Answer 15

Amygdala learns tone-shock pairing => Emotional aspect of memory

Hippocampus records the details about when and where fear conditioning occurred => Context (Generalization of fear learning to other stimuli in learning environment e.g 911, rats context conditioning)

There is also additional roles of the cortical areas in context processing of course.

Question 16

What can disrupt context memory?

Answer 16

Traumatic stress can disrupt context memory => context-free intense fear (e.g. in PTSD)

Question 17

Describe a process involving engrams and contextual fear conditioning. Evidence for the role of what brain area in what function is shown here?

Answer 17

Tag-and-manipulate

Encoding and tagging: Neuronal assembles active during contextual fear conditioning (e.g in amygdala, dendate gyrus (DG) and cortex)permanently tagged by expression of a (protein) label (engram neurons)

Storage: After training, mice return to home cage, where they do not freeze. Engram is consolidated and engram neurons become inactive.

Opsin-induced inhibition:
Optogentic (through light) silencing of tagged engram hippocampus (DG) neurons: Blocks retrieval (reduced freezing). Inhibiting DG neurons is sufficient to decrease reactivation tagged engram neurons in cortex and LA!

Opsin-induced excitation: Optogentical activation of DG neurons in new context: Freezing in new context, optogenetic activation as retrieval cue. Activating DG neurons is sufficient to induced reactivation tagged engram neurons in cortex and LA!

Diagram in notes

Question 18

Describe the process of extinction

Answer 18

Now known as extinction learnning because it is learning not to fear a CS that is no longer paired with US. It requires new safety learning (actively competes with old fear learning be inhibiting CeA).

Question 19

How does context play a role in extinction?

Answer 19

A rat can learn a fear response to a tone in cage A. If it is then moved to cage B, this fear response can be inhibited and become extinct, therefore no fear response is exhibited. If the rat is then moved to cage C and a tone is sounded, then it will likely still show the freezing response as this is not the context in which it learned extinction. There is a restriction of extinction to specific context of extinction learning which is the opposite of the generalisation of fear learning!

Question 20

What practical implication does this role of context have?

Answer 20

It can be frustrating for people trying to treat disorders such as anxiety, phobias or PTSD as there can be a frequent reemergence of fear response (exceptional persistence of fear learning) in contexts outside of which the fear response has been helped or extinguished (e.g the doctors office or therapy room.)