Multiple Memory systems Flashcards
What are the phases of episodic memory
- Short term working memory: PFC holds info in active thought. holding a conversation etc. Coordinates various brain regions. Unscathed in patient HM.
- Short term and long term memory. Physical storage substrates
like synaptic plasticity.
To remember longer than hours you need protein synthesis (late LTP), gene expression and the addition of new synapses (synaptic consolidation) - Remote memory. Systems consolidation, transformation/transfer of memory between hippocampus and other structures (or within hippo itself)
What is the standard model of “systems memory consolidation”
Prior to learning, regions are unlinked and independant.
Then During learning, hippo synapses store info (via LTP) and initiate LTM. Then systems consolidate and transfer learning to neocortical system (binding circuits together)
THen after that, a carbon copy of memory exists in neocortical regions, independant of hippo.
The memory is bound together in the neocortex.
If you were to rapidly store things in the cortex, things would get disrupted, so they have to slowly migrate there through hippo and free up storage for new memories
What is evidence for the standard model?
Multiple things of evidence, most convincing in rats about contextual fear memory. Rats are given shocks and then waited time between lesions to hippo. (wait a day or a week or multiple). Found that if they wait long enough, it doens’t impair their fear memory, but if they lesion it sooner, the rats don’t fear the chamber anymore.
Damage to hippocampus disrupts recent but not remote memories.
What is the Multiple Trace Transformation theory of memory consolidation?
There are two types of memories.
1. Episodic in hippocampus and
2. Semantic in neocortex.
The older the memory is the more traces it has (due to continued consolidation) and the more resistant to damage it is.
episodic memory is always dependent on hippocampus, but semantic memories are NOT.
Hard to measure without the right tests.
Past memories still rely on the hippo even if they happen a long time ago, but they have many more traces and are harder to damage.
How do we distinguish episodic vs semantic memories in experiments.
Looking at amount of freezing (in mice) after fear conditioning over the same period of time. If they are in a different place they don’t freeze as much. THe longer you wait, the difference goes away, and putting them in a novel environment they freeze just as much. So over time, hippocampal memory is likely ‘forgotten’ and the more general type of memory that exists is semantic.
But if you promote hippocampal memory they remember better after a month
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You don’t see this in the water maze cause you need a detailed spatial map all the time.
SOME SPATIAL MEMORIES ALWAYS STAY IN HIPPOCAMPUS
How are memories consolidated? Example.
In rats, they ‘replay’ navigational experiences when they sleep. Same temporal order than rats experienced during the day is seen replayed during sleep.
Replay originates in CA3 neurons.
Slower firing in sleep*****IS IT during sleep or waking??
Can see this activity with electrodes.
If you stimulate and mess up this areas, it interferes with memory.
Replay is important for consolidation, in both same order and reverse replay (retracing your steps)
What is hippocampal vs. striatal memory?
Hippocampal: cogntive, place memory
Striatal: habit/stimulus response memory.
Using a + maze, after 8 days, rats were using place strategy initially, then switched to response/habit strategy after 16 days.
Response: habit, turn left no matter what
Place: using spatial map, figure out where food is and turn right.
Initially cognitive requires conscious thought, but with time it swiches to habit which is more efficent.
What are the advantages and disadvantages of cognitive vs. habit memory?
Hippo: flexible, allows you to take a new route to go somewhere
Striatal: fast, automatic, unconsious.
They both lead towards the SAME BEHAVIORAL GOAL which makes them hard to sutdy.
Tradeoff: habits can lead to mistakes if applied in the wrong scenario. It can also lead to amplified habit behavior in cases like anxiety, autism, tourettes when there is more striatal and less hippocampal activity.
What is the main stress hormone in the brain?
Glucocorticoids.
Dense expression of these in the hippocampus.
Glucocorticoids are released in adrenal glands and are told to be released from brain signals which then allow it to get up to the brain. Cortisol and corticosterone in rats.
When you expreience a stressor, corticoids are elveated throughout body and brain to help you remember the experience.
Stress strenghens synapses. most of the time.
How does acute stress promote hipppocampal memory formation? Study we looked at??
Stress increased the water maze learning in rats. Colder water improved time finding the platform. Leads to more corticosterone release. - this is also shown just in injections of corticosterone.
However there is a ceiling effect of injection. Where they can’t do much better., if they’re in 19* water and get injected, it doens’t help any more.
How does acute stress impair hippocampal memory retrival?
Rats who were stressed out just before (30 mins) a test, did more poorly. But didnt see the effect 2 mins before or 4 hours after. It takes a while to elevate stress levels and they do come down after a while
Stress impairs ability to recall that memory.
What effect does severe stress and trauma have?
IT damaged hippocampus. Can’t study it as well in humans, but they do show smaller hippocampuses in patients with depression and with other disorders, AND psychological truama due to stress or other.
In rodents, we see CA3 pyramidal neurons atrophied if they were subjected to constant restraint stress.
It also reduces neurogenesis and hippocampal volume.
TREATMENTS CAN RESTORE THIS FUNCTION/STRUCTURE.
Antidepressants in humans increase number of stem cells and restore DG neuron numbers.
in rats antidepressants increase neurogenesis and can reverse the effects of chronic stress.
How does hippocampal dysfunction in PTSD and anxiety disorders work?
Cues associated with stressful experince may be tied to safe experiences that can trigger the recall of the full memory - via the synapses its connected to. SO when the the DG doesn’t do its job and properly separate the experiences, you can get improper triggering. This triggering can be helpful in the right siutation.
TLDR: impaired pattern separation can lead to generalized fear and anxiety in response to innoculous cues.
Via overlapping populations.
How does dentate gyrus dysfunction lead to generalized fear in mice?
If the dentate gyrus isn’t doing its work, it impairs pattern separation. Mice without NMDA receptors are worse at context specific fear discrimination and mice with more neurogenesis are better at context discrimination.
How does PTSD and anxiety effect pattern separation?
they are impaired, they can’t separate circles of different sizes (paired with a shock stimulus). i.e. show less discrimination between similar circles and show a startle and self reported increase in risk ratings.
hippocampus is highly active when performing this discrimination.
People with anxiety have possible impairments with hippocampus that may contribute to their ability to discriminate.
