Chapter 12: Memory Phases - Consolidation Flashcards
In what way is ultra long term memory the “final repository” for memory?
to achieve permanence, memories must be consolidated into ultra-long term memory
does this imply that memory traces must be moved/changed
retrieval to STM can also occur from this store; return to lability and reconsolidation (through LTM)
What is the adaptive power of having a “consolidation” process for long-lasting memories?
ability to modulate strength of memory trace; have the ability to “lock in” info, choose what we want to lock in or let go
What are “Flash Bulb” memories?
memories that are encoded extremely well do to emotional salience
last a long time, associated with a very intense emotion
Could activation of the sympathetic nervous system modulate consolidation?
emotional sequences can aid in memory, regardless of what type of memory it is
What is the nature of a “consolidated” memory trace?
is a “remote” engram identical to its more “recent” form?; for procedural it’s identical, for explicit memory it is highly unlikely to be identical
what is the nature of change, if any, to the physical substrate of the memory?
What is fixation?
a.k.a. cellular consolidation
the idea that activity-dependent plastic changes need to be “fixed” or made more permanent through some cellular/molecular processes
e.g. protein synthesis (translation), gene activation (transcription)
original cellular changes in learning have to be fixed in some way
relevant for both explicit and implicit memory
What is reorganization?
a.k.a. systems reconsolidation
the idea that the memory trace (engram) is changed (moved?) and becomes differentially dependent on brain structures other than the one responsible for encoding it
hippocampus to neocortex
only relevant to explicit forms of memory, particularly episodic, maybe also semantic
What is the behavioral evidence for memory consolidation?
spaced versus massed learning paradigms: by extending learning period there was less forgetting
interference (learning new material): people had a hard time not thinking of things after learning (spontaneous rehearsal), prevent this rehearsal, more forgetting, time after learning is important
What is the clinical evidence for memory consolidation?
loss of consciousness (concussion - surgery): don’t remember the sequence of events before the concussion
disrupted activity (epilepsy - ECT): cannot recall events that lead up to episode, particularly MTL, wake up confused, ECT shows temporally graded retrograde amnesia
What is the experimental evidence for memory consolidation?
post-learning manipulations of hormones or neuromodulators: can either enhance or hinder ability to remember when make manipulations in the period right after learning
post-learning influence of “offline” states (e.g. sleep): important for procedural and declarative
disruption of protein synthesis: also occurs in disrupting activity, pain synthesis dependent phase
What does all of the evidence for memory consolidation suggest?
that recent memories are labile (easily disrupted) while remote memories are stable (immutable)
What was the experiment that tested the timing dependencies for amnestic effects of protein synthesis inhibition?
train animals then give protein synthesis inhibition
give short-term test and long-term test
does inhibition interfere with STM, LTM, or both?
is timing of the manipulation (inhibition) important?
What were the results on STM and LTM of administering a drug to block consolidation at immediate time intervals?
no difference between experiment and control at STM
severe impairment of LTM function in experimental group
What were the results on LTM of administering a drug to block consolidation at immediate and delayed time intervals?
after a delay of 6 hours between test and inhibition perform like control
inhibition of consolidation needs to be delivered at a certain time after memory training
What is the post training brain region neuromodulation paradigm?
manipulation occur following training
no interference with motor, cognitive abilities in task itself during training/testing
What was the Morris water maze and intracranial infusion of amphetamine experiment of post-learning memory-modulating manipulations?
spatial version: dropping rat at random spot, fixed platform below surface, need to use spatial cues to figure out its location and path to platform, only get one training session
cued version: learn that a cue signals the platform, then escape
What were the results of the Morris water maze and intracranial infusion of amphetamine experiment of post-learning memory-modulating manipulations?
spatial version: enhancement with HPC and amygdala infusions of amphetamine
cued version: enhancement with striatal and amygdala infusions of amphetamine
suggests that activating amygdala is important for solidifying either type of memory
How do stress hormones modulate consolidation?
stress hormones (adrenaline & cortisol) modulate consolidation by direct brain (& amygdala) activation
amygdala lesions or infusions of adrenergic antagonists block these effects
amygdala infusions of adrenergic agonists mimic these effects of amygdala activation, memory enhancement in post learning environment
How do emotions and drugs that mimic endogenous responses to emotion enhance memory consolidation?
protein synthesis?
blockers of protein synthesis inhibit memory consolidation when applied in the post-training period as well
de novo protein synthesis hypothesis of long-term memory: need new proteins to be expressed
enhanced neural activity: replay and reactivation of ensembles in post-training period
What makes an old memory different from a new one?
time: longer the time, more able to retain
recall frequency/probability: recollecting, older memories have been rehearsed longer
intervening experiences
Is the HPC the location of the consolidated engram?
experimentally, HPC damage has been suggested to affect newly learned material more than material learned in the distant past
implication: HPC is needed only to lay down and recall recent memories, but is not needed to recall remote memories
longer delay between learning and lesion –> less impaired
when you lesion HPC you get impairments in HPC dependent memories
where are these remote memories located? what structure are they dependent on?
What is the controversy regarding temporal retrograde gradients?
previous studies didn’t have lesions of the full HPC in rats, a quarter was still left
gradient may not exist if only lesioning a small part
systematically lesioned the entire hippocampus
if you damage HPC (no matter the delay) can’t access info
not sure if you have the memory of your childhood, or the memory of a picture, video, or your parents saying it
are remote memories of the HPC dependent on the HPC, or do they become something else, a story?
What is the hippocampal involvement in both recent and remote memories?
precise temporal control of hippocampal activity during recall
recent and remote memories depend on the immediate activity of the HPC
interaction between hippocampus and prefrontal region to retain info in the absence of HPC
What was the optogenetics experiment to test the hippocampal involvement in both recent and remote memories?
infect neurons with viral vector for opsin, imbedded in membrane, allow them to get excited by light (movement of cations)
pumps Cl- into cell, inhibits firing
inhibit activity of CA1: stop expressing fear
after a week: CA1 inhibition showed no fear
prolonged CA1 inhibition: gradually express fear, reactivate memory, looked at anterior cingulate cortex
