Elsey Paper - Reconsolidation as treatment

Question 1

What is reconsolidation in the context of memory?

Answer 1

Memory reactivation can induce a “labile period”, during which previously consolidated memories are sensitive to change, and in need of restabilization

Question 2

Of what does memory labilization appear to be the result?

Answer 2

Interplay of:
- Learning history
- Reactivation
- Individual differences

Question 3

What do the seeming causes of memory labilization pose?

a problem

Answer 3

A problem for translating this into effective clinical interventions

Question 4

Which four types of exposure therapy was mentioned in Elsey et al., and what do they mean?

Answer 4

• In vivo = confrontation with external stressors in real life
• Imaginal = exposure to feared situations/memories through the imagination
• interoceptive = exposure to feared internal senstations
• VR = VR as exposure mimicking real life situations

Question 5

What is extinction training and what is a problem with it?

Answer 5

• extinction training is re-exposure to conditioned stimuli without the aversive (US) present
• It does not cause unlearning of the original fear memory and only creates a new inhibitory memory > resurgence of the old memory can thus occur

Question 6

What is a proposal for exposure that goes beyong simple habituation in patients?

Answer 6

Focus on violating the patient’s expectations about negative outcomes that might occur upon exposure to the CS

Question 7

Why may negative reinforcement during extinction be useful?

Answer 7

Possible reduction of the disparity between the new learning and the original memory (potentially acting directly on the original memory or meaning that later negative outcomes don’t automatically activate the maladaptive memory, because the new one also contains aversive experiences)

Question 8

A counterintuitive implication of exposure treatment?

Answer 8

Providing occasional reinforcement during extinction might reduce spontaneous recovery

Question 9

What is spontaneous recovery in the context of conditioning?

Answer 9

It is what happens when a “rest period” (the CS is no longer presented) happens after extinction > the CR comes back in full force, despite previous extinction

Question 10

Why is a focus on inhibitory learning and competing memory traces important for exposure therapy?

Answer 10

It could serve to enhance treatment outcomes/understanding

Question 11

Focus of the Elsey paper?

Answer 11

focus on attempts at disrupting reconsolidation of maladaptive memories in anxiety and trauma-related disorders through pharmacological means, and particularly the use of propranolol in humans

Question 12

What is the dominant model of memory formation?

Answer 12

memories transition from a short-term and relatively unstable trace to a
more persistent long-term form

Question 13

What is consolidation, within the context of memory?

Answer 13

Memory transition from short-term to long-term

Question 14

By what is consolidation thought to be mediated?

Answer 14

protein synthesis dependent synaptic changes

Question 15

What do protein synthesis inhibitors (PSIs) do?

Answer 15

Prevent the expression of long-term memory when administered shortly after learning

Question 16

How do PSIs work with consolidated memories?

Answer 16

They seem resistant towards PSIs

Question 17

How can PSIs proof useful when a memory is already consolidated?

Answer 17

If the memory is reactivated, administering PSIs shortly after reactivation might prevent the later expression of long-term memory

Question 18

Why are PSIs not currently used for humans?

Answer 18

Due to the range of side-effects

Question 19

How does propranolol work for reconsolidation?

Answer 19

It blocks beta-adrenergic receptors, believed to indirectly inhibit protein synthesis by halting noradrenaline strimulated CREB phosphorylation in the amygdala

I’m not sure if you need to know this exactly, moreso just remember that propranolol indirectly prohibits protein synthesis, which seemingly provide the same effect as PSIs

Question 20

What does the potentiated startle response indicate?

Answer 20

Appears to track emotional valence (pleasentness/unpleasentness) of stimuli

Question 21

Differentiated fear potentiated startle (FPS)?

Answer 21

development of potentiated startle of stimulus paired with shock (CS+) relative to the unpaired stimulus (CS-)

Question 22

Results for the study with potentiated startle responses & propranolol administration? (3)

Answer 22

• Participants retained their declarative memory for the conditioning procedure
• Participants receiving placebo + memory reactivation OR propranolol alone = still displayed FPS
• Participants receiving propranolol + memory reactivation = abolisment of FPS

Question 23

How did the FPS fare in the propranolol + memory reactivation group after follow-up (which included things like reinstatement)

Answer 23

• FPS was not reinstated by unsignalled shocks, nor did it recover when stimuli were presented in a different experimental context or through the mere passage of time
• FPS did not re-develop any faster during re-conditioning than initial learning (no saved memory traces)

Question 24

What does FPS not re-developing any faster during re-conditioning than initial learning indicate?

Answer 24

Reduction in startle response is likely not attributable to an inhibitory process like extinction

Question 25

A general conclusion that can be made (from this paper) about extinction vs. reconsolidation procedure?

Answer 25

That reconsolidation procedure is stronger than extinction

Question 26

What further support is there for propranolol only disrupting the affective component of the memory and not retrieval?

Answer 26

Differential skin conductance (thought to equal representation of fear memory) remained intact, as well as expectancy ratings

Question 27

Propranolol in PTSD? (3)

Answer 27

- propranolol administered so as to interfere with reconsolidation after exposure to traumaticimagery significantly attenuated physiological responding to the imagery relative to placebo - Although another study found no differences between pro. + reactivation & only pro. - In general, mixed findings with small sample sizes & lack of account for non-specific effects

Question 28

Propranolol in specific phobias?

Answer 28

Seemingly effective

Question 29

Current likely hypothesis on the workings of reconsilidation? (2)

Answer 29

- it may allow for memories to be updated, thereby retaining their relevance and usefulness in a changing environment - thus reconsolidation (if this is true) would be most reliably induced by memory reactivation that in some way adds to or indicates the need to update the memory

Question 30

How do prediction errors play a role in reconsolidation?

Answer 30

The susceptibility for amnestic effects of PSIs seemingly depend on going against prediction errors (e.g., reinforcement at a different time than expected from training)

Question 31

How does memory expression play a role in reconsolidation?

Answer 31

It is not necessary nor sufficient for reconsolidation

Question 32

How do prediction errors support the hypothesis of reconsolidation being a memory that is updated? (2)

Answer 32

- If unreinforced CS presentation, but not reinforced, allows for reconsolidation - this indicated that the outcome differing from the prediction is what allowed the reconsolidation (i.e., updating was necessary) - The same counts for reinforcement differing than expected > updating is necessary in the face of unexpected results **I.e., prediction errors, not the absence of reinforcement/memory retrieval, is necessary for the destabilization of conditioned fear memories** | **having the device that gives the reinforcement present is necessary**

Question 33

Why is prediction error difficult to recreate in clinical practice?

Answer 33

The learning process is often vague or even unknown, the clients also often have a large range expectations- not all easily destabalized nor directly relevant to the fear memory

Question 34

What solution is proposed for the difficulty for prediction error destabalization in clinical practices?

Answer 34

A focus on the most salient fears to design the reactivation session

Question 35

What is something, besides violation of expectations, that may aid prediction errors in reconsolidation?

Answer 35

Learning of additional information is learning has not reached max (? they used a weird af word in the original sentence). I.e., novel experiences with feared stimuli could also aid destabilization

Question 36

Why is prediction error not necessarily sufficient for reconsolidation?

Answer 36

Because it is still dependent on things like the length of reactivation or extend of the prediction error

Question 37

How do longer vs. shorter windows of reactivation affect the fear memory?

Answer 37

Longer = extinction and shorter = reconsolidation (seemingly)

Question 38

"These studies demonstrate that the induction of reconsolidation is a balancing act" what is meant by this?

Answer 38

without prediction error, memory is not labilized and made vulnerable to amnestic agents, but with extended reactivation and multiple prediction errors, destabilization does not take place and extinction may even occur instead

Question 39

How is the ecological validity of the experimental models for the reconsolidation looking?

Answer 39

eh, not yet clear that there are sufficient parallels between true anxiety disorders and the experimental paradigms that have been investigated thus far - Simplistic, recent and unimportant memories (as opposed to complicated, long-lasting and deeply ingrained memories often seen in anxiety disorders/PTSD)

Question 40

What is problematic about second-order conditioning?

Answer 40

In clinical practice, it is not always clear which fears are central to a client, and which are peripheral- if peripheral fears are used, this likely will not actually reconsolidate the central fears (and thus leave the client with suboptimal treatment outcomes)

Question 41

What is a problem with using measures like the fear potentiated startle?

Answer 41

That it does not account for subjective experience (or at least, not necessarily so) - research that accounts for subjective experiences after propranolol are limited as of now

Question 42

Four criteria presented for the demonstration of reconsolidation for human research?

Answer 42

- Interaction between memory reactivation and the manipulation (e.g., propranolol) - Time dependent effects of the manipulation (manipulation should not have the same effect inside reconsolidation window as outside) - Memory specificity (it should only affect reativated memory trace) - Dissociation of immediate and delayed effects of the intervention (short-term traces may be retained)