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two types of memory consolidation

Intracellular/Synaptic Consolidation - refers to processes within individual neuron that stabilize changes in synaptic weighting

Systems Level Consolidation – refers to consolidation that is dependent on the interplay of activity across brain areas (usually refers to interplay between medial temporal lobe structures and neocortex)


what does synaptic signal trigger?

- covalent modifications
- incorporation of new proteins into synapse or remodeling of existing synaptic structure
- epigenetic regulation of protein synthesis


what does the HM case show about system level consolidation?

Suggests that (a) declarative memories are consolidated, and (b) that MTL plays a role in this process, but that (c) MTL is not the ultimate repository of such memories;

This suggests that new memories can be briefly “stored” outside of MTL, but that without the MTL’s involvement, these memories are quickly lost


one theoretical model which attempts to explain role of MTL structure in the consolidation of declarative memories

neocortex: high-capacity but slow-learning system
MTL: fast-learnning

Basic idea is that:

Some types of learning (e.g., declarative memories) induce changes in neocortex (initially weak memory “trace”) as well as medial temporal lobe (MTL) structures (initially strong)

Neocortex is a permanent site of memory storage. This implies that new memories have to be integrated with old memories. This is assumed to be a delicate process – one that can potentially lead to “catastrophic interference.” As a result, it proceeds slowly. So the neocortex is a high-capacity but slow-learning system. Once memories are firmly embedded in neocortex, they are “consolidated.”

MTL, on the other hand, is a temporary site of memory storage (spatial memories and episodic memories may be exceptions). Perhaps for this reason (i.e., no need to integrate new with old), it is a fast-learning system (albeit with limited capacity).

Over time, presumably during "off-line" states when the brain is not actively processing other information (sleep states have received much attention but quiescent waking states may also be involved), interactions between the MTL and neocortex take place that are essential for the long-term storage of these memories outside the MTL. One idea is that the MTL replays elements of experience to the neocortex, and that with enough of this type of covert rehearsal, the neocortical trace is strengthened to the point where it can exist independent of the MTL.


Donald Hebb's theory (first biologically explicit model)

learning event;
initially coded and maintained by self-sustaining "reverberatory" electrical activity;
this electrical activity induces structural changes


first published evidence for consolidation processes in animals

T-maze with elctroconvulsive shock

slide 13


describe post-training treatment experiment and its advantage

puromycin (protein synthesis inhibitor)

Mouse placed in Y-maze. Footshock is delivered to start arm and also to left arm. Rat escapes from the start arm and over the course of several trials, learns to always escape to right (i.e., to the non-shock arm).

Puromycin infused either 1 or 40 days later and rat tested 3 days after that. long-term memory disrupted after 1 day, while intact after 40 days.

No possibility that observed deficits are due to effects on sensory or other processes that affect learning (e.g., reduced shock sensitivity) because treatment is delivered after learning.

If treatment only works when given soon but not long after training, the behavioral effects cannot readily be attributed to effects on memory retrieval or expression at the time of testing.


describe pre-training treatment and its advantage


puromycin infusion, then 5 hours of training. STM test 15 min after training (retention normal), LTM test 45 min after training (retention impaired).

A unique advantage of this approach is that it directly tests prediction that a given treatment interferes with memory consolidation rather than acquisition (i.e., because it looks at short-term memory as well as long-term memory and tests prediction that treatment interferes with one and not the other).

If short- and long-term memory are differentially affected, it is unlikely that this is due to treatment effects on sensory or other processes needed for learning because both short- and long-term memory would be disrupted by impaired learning (i.e., if rat could not feel shock, then there would be no evidence of short- or long-term memory).


describe Walter Cannon's "Emergency Theory of Epinephrine"

epinephrine vs glucocorticoids

slide 23/27


describe the "rescue" experiment of epinephrine

retention test (measure latency to re-enter shock compartment)

slide 24


describe experiment studied memory modulation in people

placebo vs propranolol pill
neutral story vs high-arousal story

better recall for high- vs low-arousal items;
propranolol prevents enhanced retention of high-arousal story elements;
patient B.P - an individual with bilateral lesions restricted to the amygdala - does not show enhanced retention of high-arousal story elements


describe lick suppression test

control group: good retention
ECS group: poor retention
delayed ECS group: good retention
delayed ECS group with re-activation: poor retention

Rat trained to lick water bottle spout to get water;
Rat receives tone-footshock pairings (Pavlovian fear conditioning)

Determine rate of spout licking without tone (high;)
Determine rate of spout licking with tone (low in normal animals provided that tone had been paired with shock)

Lick Suppression by tone is the measure of fear


experiment to show that sites of neocortical reorganization critical for remote spatial memory

Rats were trained to remember which 3 arms of an 8-arm radial maze were always baited with food. Retention was tested either 1 or 30 days later.

Rats were euthanized afterwards and brains were processed to visualize the immediate early gene Zif268 (used as a marker of neural activity (left). Relative to the Day 1 test, retrieval from long term memory was associated with increased activation of neocortical areas and decreased activation of hippocampus. Similar results were found using 14C[2DG] as a marker of metabolic activity (data not shown).

In other groups, lidocaine was infused into one of these same areas (used to inactivate neurons) just before testing. Inactivation of hippocampus disrupted short-term but not long-term memory. Inactivation of frontal or cingulate cortex disrupted long- but not short-term memory.