Summary: Ndpd

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• 1 NDPD

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• HC PTSD: military study

  Exp: 2 groups: military training & Afganistan militaries group
  Task: angry and fearful halves need to be matched with bottom halves (emotional processing task)
  Temporary upregulation: Afganistan group showed increased upregulated amygdala reaction during the emotion-faces task
  In 'normal' people: upregulation normalises over time
  Anxiety disorder: amygdala activation stays increased (also in GAD, etc)

• HC PTSD: (Healthy) memory consolidation: Cellular and system level

  Encoding -> Consolidation -> Retrieval
  Gradual stabilization and integration of initially labile memory into long-term storage
  Cellular level: Higher synaptic efficiency + neuronal communication
  System level: Reorganisation of neuronal networks   
  Time and sleep dependent

• HC PTSD: Hippocampal binding theory, example HM, dependent on (2)

  1. Hippocampus binds all separate experiences and their memory traces together in the cortex (strengthens the connections).
  2. Cortex traces become more dissociated from hippocampus over time (still interconnected)  
  3. Memory traces will form a cortico-cortical connection network (Hippocampal lesion would not affect this memory)
  HM patient: hippocampal independent memories were intact (old memories)
  Traces becoming independent of hippocampus is dependent on time and sleep!

• HC PTSD: Emotional memory, influence of Amygdala during 3 phases of memory

  Influence of amygdala (AM):
  1. During encoding: AM 'tags' emotional event: influences the hippo-cortex interplay. AM becoming more active needs (nor)adrenaline and cortisol (=stress)
  2. During consolidation: AM imposes theta-rythm on hipp-cortex interplay, making cortical connection forming earlier
  3. During retrieval: (from article): Sensory aspects (smells, sounds, etc) of memories get retrieved involuntarily ('intrusions')

• HC PTSD: Traumatic memory consists of (2) and role of sleep

  Traumatic memory: 
  1. representations in certain order and context (core memory)
  2. affective tone: emotions/mood of the moment
  During sleep, memory becomes dissociative of emotional state. PTSD re-experiencing the memory does not decrease, same emotional state as if it happened. Problem in decoupling, possibly during sleep.

• HC PTSD: Sleep replay. Exp with rats. Sleep needs (3) for replay.

  Exp rats: 1. walking in environment. 2. sleep: place-hippocampal cells at random order become active. 3. walk. Place-specific hippocampal cells become active and at order. 4. Sleep. Place-specific neurons become active and in same order as orientation memory task. COncl: memories are replayed and ordered during sleep. First night is crucial, memory is not ordered and still vulnerable. 
  Sleep needs: 1. Neocortical slow oscillations 2. thalamo-corticol spindles 3. hippocampal ripples (reactivation)

• HC PTSD: Sleep and odor exp. fmri results and effect of sound

  Exp odor: odor during memory task. Odor during sleep to stimulate replay. Results: better subsequent memory. (Not during REM or waking, only for hipp-mediated memory, not procedural oid)
  fMRI:
  Odor activates hippocampus
  
  (Sound: no better subsequent memory, but better hipp-cortex interplay)

• HC PTSD: Targeted memory reactivation

  Sounds during slow-wave sleep to boost memory
  (Unlearning implicit social biases during sleep)
  Stimulus specific enhancement of fear extinction during slow-wave sleep

• HC PTSD: summary consolidation (5 steps)

  1. Memory initially hippocampus/MTL dependent
  2. Gradual transfer to cortex with time (and sleep)
  3. Memory strengthens, emotion lessens
  4. Replay of memory traces in hippocampal-cortical loop
  5. Targeted memory reactivation to boost consolidation

• HC PTSD: Dual representation theory

  C-reps = cortex representation at cortex level (autobiographical) both voluntary and involuntary retrieval
  S-reps = sensational representation amygdala (sensations, physiological) not flexible. Intrude memory automatically and involuntary (i.e. nightmares, flashbacks)