Memory Flashcards
Amnesia
Memory loss or issues with memory formation
Retrograde Amnesia
Forgetting the things that happened prior to a neurological issue/TBI (more common with recent memories)
Anterograde Amnesia
Inability to form new memories
Patient HM
Received a bilateral medial temporal lobectomy to treat his extremely severe temporal epilepsy.
Removal of his temporal lobe/cortex came along with removing the vast majority of the hippocampus.
What were Patient HM’s issues with memory?
Remember: Removal of HM’s temporal lobe/cortex came along with removing the vast majority of the hippocampus.
HM’s short term/working memory was preserved, but he could not consolidate these memories into his LTM.
The hippocampus is not where LTMs are stored but the hippocampus is what consolidates the memories.
HM’s long term memory was not impaired for which three things?
- Mirror drawing test (only using mirror visual feedback to draw) - he improved at the mirror drawing test each time he did it, but had no conscious memory of the task
- Pavlovian conditioning - he has a reflex but does not know why
- Priming - Occurs after patient HM sees a list of words even if he cannot remember the list
Explicit memory:
Conscious or unconscious?
Effortful or automatic?
What parts of the brain is it processed in?
What are some examples? (Two types)
Something you would be able to consciously remember/recall (declarative).
Effortful.
Processed in the hippocampus, frontal lobes, and temporal lobes.
Examples:
Semantic Memory: Facts and general knowledge (e.g. Content from PSYC 301)
Episodic Memory: Personally experienced events (e.g. Family holidays).
Implicit memory:
Conscious or unconscious?
Effortful or automatic?
What parts of the brain is it processed in?
What are some examples?
Cannot typically be consciously probed (nondeclarative). AKA muscle memory.
Automatic.
Processed in the cerebellum and basal ganglia.
Examples: Motor/cognitive skills like riding a bike; classical conditioning; space/time/frequency (e.g. How many times have you ate pasta this month, you can give a good estimate).
Space/time/frequency - a “cached value”
Which part of the brain plays a large role in classical conditioning?
The cerebellum
Hippocampal Indexing Theory
The hippocampus acts as an index, and that indexing allows us to reactivate networks.
The network eventually becomes so strong that the hippocampus does not need to reactivate the pattern/recall memories, as the connections within the cortex itself will be sufficient. This explains why more recent memories are more susceptible from hippocampus damage than old memories.
Another implication: It seems like in healthy humans, the hippocampus always plays a role in episodic memories (narrative events, sequential events, etc.)
LTP Rat Study (Explain The Study and Its Key Findings)
LTP is measured via four electrodes in the cortical structure of the hippocampus.
There are two “stimulating” electrodes and two “recording” electrodes (one inside, one outside the cell).
One stimulating electrode provides a constant weak stimulus to the hippocampus, and one’s job is to briefly provide a strong stimulus.
By weakly stimulating axons, a baseline amount of neurotransmitters are released. Those NTs bind to ionotropic receptors, some ions come in to the receptors and cause EPSPs.
You measure these EPSPs (for ten mins) to assess the “baseline” strength and frequency.
After ten minutes, a very strong stimulus (known as a tetanus) kicks in - well above levels of stimulation you would find in the natural world (but you will see similar processes occur with less intense stuff)
Strong stimulus/artificial stimulus (tetanus) - suggests something really intense just happened - neurons ‘fire together to wire together,’ then you go back to the baseline weak stimulus… you will notice the EPSPs are stronger than they were before!
This might be more detail than what is tested, but better safe than sorry!
What are the steps that allow long term potentiation to happen?
Discussing the chemical process, not the structural or functional changes that come after, that would make this flashcard extremely long.
- NMDArs on the dendrites of hippocampal neurons are highly stimulated by greater amounts of glutamate being released by axons.
- This means the dendrite membrane depolarizes (becomes more positively charged).
- This positive membrane pushes against the positive magnesium ions in the NMDArs (these magnesium ions are at a binding site on the NMDAr that blocks the NMDAr channel).
- This pushes the magnesium ion OUT OF the NMDA channel, making it so sodium and calcium can flow into the neuron.
- This calcium signal is what drives/triggers the LTP process - both the immediate changes in the dendrite, and long term changes that send ‘messages’ to the cell that go all the way to the nucleus.
So, LTP is a calcium-mediated signal process!
Wernicke-Korsakoff’s Syndrome
1. Brain Region Affected/Damaged
2. Pathogenesis (Causes)
3. Symptomatology
3.5. Symptomatology For Alcohol-Induced WK’s Syndrome
Brain Region: Anterograde amnesia, caused by damage to the medial diencephalon (medial thalamus), NOT the hippocampus.
Pathogenesis: Can be caused by discrete damage or thiamine (vitamin B1) deficiency (this can happen due to general diet or extreme alcohol intake).
Symptomatology: Korsakoff’s leads to severe anterograde amnesia with some retrograde amnesia with recent events. Note that for alcohol-related damage, Korsakoff’s more closely resembles a neurodegenerative disorder with aspects of Parkinsonism and Dementia.
How can extreme alcohol use lead to Korsakoff’s Syndrome?
Two key factors.
- Alcohol blocks the transporter for thiamine (which gets thiamine across the blood brain barrier), and the thiamine does not get into the brain.
- People who drink a lot of alcohol eat less on average due to how calorically dense alcohol is.
Thus, the brain is left in an extremely depleted state when it comes to thiamine.
Very Not Fun Fact: These cases of Korsakoff’s are typically MUCH more severe.
