F. Learning, Memory, and Amnesia - Part 3 Flashcards
What are the 2 sys that provide ACh to the rest of the brain? Where do they project?
- Cholinergic basal forebrain -> cortex
- brainstem cholinergic sys -> thalamus, basal ganglia, brainstem, cerebellum, spinal cord
What causes the release of ACh?
arousal/attention grabbing stimuli
What are the 2 types of cholinergic receptors? Include the following info
a) ligand or metabotropic?
b) how many subtypes?
- muscarinic
a) metabotropic
b) 5 subtypes - nicotinic
a) ligand
b) +40 subtypes
why is ACh so important of memory
It is easier to encode info about a stimuli that you are attending to and ACh is the NTX released when something arouses your attention
What is scopolamine and how does using it help researchers find out more about the effects of ACh on memory?
muscarinic receptor antagonist. This is one of the receptors that ACh binds to. When it is injected in rodents during the different phases (sample, 24h delay, choice) we can observe how the rat reacts.
As expected if scopolamine (antagonist for muscarinic receptors) is injected right before the sample phase the rat exhibits memory impairment. However, it appears to have memory improvement if injected right after the sample phase before the 24h delay. Why could this be?
during the acquisition phase (sample) the rat is encoding the information about the obj therefore it is in an active stage where it is easily disturbed. Therefore, if you inject the antagonist right after the info is encoded it prevents anything else from disturbing that info until it is properly encoded resulting in memory improvement.
T or F - if you block muscarinic receptors using nicotine it impairs memory during the acquisition, consolidation, and retrieval phase
F
- scopolamine = muscarinic receptor antagonist
- impairs acquisition
- improves consolidation
- no effect on retrieval
Researchers suspect that administering nicotine (nicotinic receptor antagonist) improves object memory acquisition in rats. How could one test this?
Rats have the ability to remember after 24h however not after 72h therefore if you extend the delay to 72h normal rats will not be able to remember. Then you inject the test gr w/nicotine and see the results. This should show no memory impairment in the test gr compared to the control group. (assuming the hypothesis is correct)
How does the nicotinic receptor relate to those who have Alzheimer’s disease?
Those w/ AD tend to have a low number of nicotinic receptors which bind to ACh.
Draw the reactivation-induced memory modification cycle and include the following terms; stable, reconsolidation, memory weakening, reactivation, destabilization, labile, and memory updating.
a) Describe each phase in the photo
b) What is MK-801?
c) why is the MK-801 injected there?
a)
- sample phase = the first time the rat is encoding the obj
- reactivation phase = the rat is reminded by the obj
- choice phase = the rat is tested to see if it remembers the obj
b) NMDA receptor antagonist
c) testing to see if MK-801 blocks memory reconsolidation not encoding of memory so it must be right after the reactivation phase (right after the memory is reactivated)
This graph shows the results when MK-801 was injected into the rats during the object memory destabilization experiment where memory is reactivated. Why is there a ‘no reactivation’ and ‘reactivation section’?
The pt of the no reactivation phase is that the injection of MK-801 is not interfering w/ just regular consolidation as it has no effect when the rat is encoding the information for the first time. However, the rat shows severe memory impairment right after reactivation has occurred. This proves that MK-801 blocks memory reconsolidation but not consolidation
If cues can be used to reactivate old memories destabilizing them how come we don’t usually forget strong or really old memories?
Boundary conditions = some strongly encoded or remotes memories will resist destabilization in order to keep that straightened memory
If boundary conditions help strong/remote memories resist destabilization how do we upgrade or strengthen those types of memories?
novelty-induced destabilization = presenting a novel, stimulus in addition w/ cues to remind the subject about memory is the only way to put these strong/remote memories in that destabilized state
Describe DREADDs -2
a) designer receptors exclusively activated by designer drugs
b) an artificial receptor that is surgically administered in a model and only reacts to artificial compounds that act at hormones/NTX
This graph tested the effects of cholinergic transmission during the reactivation phase of memory using the DREADD agonist C21 and the NMDA receptor antagonist MK-801. We already know that blocking NMDA receptors block memory consolidation so why is it included? When MK is administered w/ C21 what do the results show?
a) It is there to prove that reactivation is occurring as the memory will only be impaired if reactivation is making the formed memory unstable.
b) They show memory improvement compared to when only MK was administered showing that encouraging the release of ACh blocks the reactivation of memory.
Describe the following parts of this image
a) the 48h delay
b) C21
c) MK-801
d) the reactivation phase is different from the sample phase
a) for rats a delay of 48h will lead the memories to become remotes rather than long-term memory
b) the DREADD agonist-modified muscarinic receptors for ACh
c) NMDA receptor antagonist - DEC LTP
d) reactivation stage contains both the old obj as well as novel-induced stimulus (the carpet) in order to encourage the destabilization of those remote memories
