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53 Cards in this Set
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define: LTM, explicit, implicit, episodic, semantic, procedural, non-procedural (and how they fit together) |
long term= associations between infos that get recorded in the brain after you stop consciously attending Explicit = conscious long term memory- can say them out loud. AKA declarative memory in humans bc we can speak explicit can be: episodic memories (collection of past experiences that can be explicitly stated: who what when, where how emotions etc.) and semantic memories (common knowledge, facts, ideas, concepts, basic facts) Implicit= - previous experience alters futur behaviour without conscious awareness of what was learned types of implicit= procedural and non Procedural memory= memory for the performance of particular types of actions, probably accomplished with reinforcement learning strategies and dopamine signalling. This is a type of implicit memory non-procedural=- like chicken pox, your immune knowns how to deal with it once it sees it once, and this is unconscious. if you flash images under level of consciousness then shock them, they will have psychophysical responses to perceiving those images consciously later |
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Hippocampus is essential for what memories? |
Hippocampus is essential for explicit memories - semantic info is stored separately form episodic- when you think of semantic info, you dont remember where you actually learned it - semantic memories may become hippocampal independent over time |
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info comes into hippocampus through ___; what happened to HM? |
the dentate gyrus to CA3 and then CA2, CA1; bilateral hippocampal lesions, had some retrograde amnesia and anterograde amnesia but could form new procedural and emotional memories |
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how do they think the neural circuits in the hippocampus work to encode memories> |
-it seems that ensembles of discrete neurons spread through the hippocampus are what encode specific memories. -Discrete ensembles of hippo neurons are active at any given moment time. As time passes or you more around, different cells become active. -Some neurons are very likely to be active when an animals in one place vs another |
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How can/do we use optogenetics to stimulate specific memory engrams (the specific neurons that encode a place for ex.) |
- we could put ChR under control of an IEG like cFOS but as the day went on, ChR would be expressed in every neuron in the brain - in bacteria, tTA is a gene transcription fator that promotes expression by binding to tTA promoter TRE (not in mammals) - doxcycline is antibiotic that binds to the tTA and stop it from promoting gene expression - so they make a mouse where this tTA will be expressd along with the cFOS. and then this tTA will drive expression of ChR - so cFos will drive expression of ChR but only in absence of dox |
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If you put the mice on dox their whole life off dox and in a novel room, what do you find? |
- you see 2-3% of hippocampus neurons active - this is regardless of footshocks or not - you can label these by linking ChR to GFP - the ChR stays active for a few days and you can stimulate these neurons selectively |
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Once you label these 2-3% of neurones in the hippocampus that responded to context B (shock), what happens when you stimulate them in another room A? |
if you stimulate the neurons that were active in the shock room, the animals start to freeze, show fear even though they were never shocked there (if the mice were not shocked in room B then putting them back in room A had no effect on behaviour) also control animals had no reaction to room A |
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Describe the valence switch experiment |
- mice on dox, give ChR to the DG of hippo or to BLA (separate conditions) - mice taken off dox and put in either fear (shocks) or reward (female mouse) condition - regardless of condition, about 2-3% of hippo cells and 2% of amygdala cells active in trials are labelled with mCherry (like GFP) - put in a box, see which side they prefer/avoid= baseline - then off dox, put in shock or reward condition - back in box, activate the neurons labelled during shock when they are in the preferred side vs reward neurons when they are in the avoided side
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Results of the valence switch experiment |
- when the neurons in the DG or amygdala active during shocking are activated, the mouse not avoids side associated with it (the one that was originally preferred) - when the reward neurons are stimulated, we see place preference from the originally avoided location |
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can we rewire neurons to change their valence? |
- take mice off dox, put them in room and shock. - label these neurons (in hippo + amygdala) - put mouse in with female mice (reward) and stimulate those neurons -in the place preference/avoidance box, the mouse that used to avoid the side that stimulated these neurons now avoids less or prefers it, but ONLY for the hippo DG neurons, not the ones in the BLA! (although it does become slightly less aversive, they dont get 'rewired') - the opposite works too, activating the rewarding neurons when they are ebing shocked causes these neurons stimulation to become aversive- but only the hippo neurons, the amygdala ones stay pleasurable
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What is a limitation of the study design with the place preference/aversion |
the baseline measurements- maybe they ended up exploring the side they had originally avoided bc they hadnt explored it yet and they wanted to... when they redo it with this in mind, they see less of an effect-the hippo becomes less aversive (and maybe a little rewarding), but amygdala didn’t show much change |
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How do mice act when they are receiving photo stimulation of positively-valenced ensemble of neurons and being foot shocked at same time? What happens if you return the mouse to the shock room after? |
- for controls, 70% if the time is freezing. But for the ones being stimulated, they freeze less - if you put them back after, the control animal still stays frozen, but the animals who had stimulation of positive neurons freeze less- fear memory less pronounced |
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The DG neurons in the hippocampus project to other places to form emotions. Are these projections actually rewiring as well? (and how did they do this) |
- for ex. the BLA neurons that show activation when you activate the DG- not a direct connection, but through a network -Give virus with with cherry and chR (the amygdala will not be stimulated, the cherry ChR is just to see which is active) to the BLA and the DG - take off dox and put into foot shock room, label neurons both in DG and projections to BLA -put mice in positive situation and stimulate the DG neurons to rewire them - 18% of the BLA cells are active when the /\ASK ABOUT THIS |
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what is the difference between the valence associated with hippo memory engram and the amygdala neurons? what does this appear to mean? |
- hippo neuron group can have valence bidirectionally reversed - when the valence changes, the projections downstream changes (at least in the amygdala) the amygdala neurons though, seem to be hardwired to drive either fear or reward associated with behaviours -it appears that the hippo causes emotions by activating the amygdala |
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Place cells; Border cells; grid cells- how do they differ? |
Place cells- neuron fires everytime the animal is in a certain spot- they are direction specific! Border cells - this neutron always fir when the animal is close to a wall Grid cells- the neuron fires in a periodic, gridlike pattern in the space
*place cells align with a location in a room and when you go to a different room, they remap. Grid cells and border cells maintain their properties, although grid cells also remap position= place cells distance= grid and border cells direction= head direction cells |
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Describe the Grid cells firing patterns and combinatorial power |
- size of each grid-based hotspot and difference between them remain constant in any room, per neutron. But different neurons may have different grids - also in dif environments, the cells grids seem to "rotate" - arranged as semi-indepenedent modules which rotate on own, which creates combinatorial power |
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When may a grid cell remap? |
-chunking- certain period of time will have stable grid and place cells, but over time the grid and place cells may remap based on other cues in the environment. - for ex. internal states can affect this-if you go in a room often hungry vs full, there may be dif maps. -putting a ball in the centre of the room may also be enough to cause the grid cells to remap |
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Hippocampal "time cells" describe experiment showing them |
- fire whenever a certain amount of time has passed -had animals run through a maze but would have to stop and run on treadmill for ten mins. there were neurons that fire at intervals in passing time, even though their position was remained constant |
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What is map formation? How does it relate to explicit memory formation? |
-When exploring a new environment you must rely on path integration but after it is well explored, then you use a cognitive map -semantic memory formation works similarly... as people go about life, events are recorded as episodes which are egocentric. Over time, brain extracts semantic memories and it becomes allocentric. - perhaps the neuronal algorithms underlying navigation in real life and mental space are the same. |
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How can we record the activity of hundreds of hippocampal neurons over weeks? What kind of GcAMP is used? |
- viral delivery of GcAMP to CA1 of hippo - place a microendoscope, a 2 gram microscope very sensitive to light and very small, above area - essentially videorecord the fluorescence ;
The authors are using the third gen GCAMP protein which only produces detectable fluorescence if 3 action potentials occur in rapid succession. It was slow to decay (>100ms). Now we have gen 6 which are fast, sensitive, and bright - they will fluoresce with one AP and decay fast |
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Trained mice to run back and forth on a track for water, then removed the water and had 5 imaging days with 50 trials. What did they find in CA1 neurons? (What are the numbers?) (5) |
- each mouse had 3000 neurons recorded - 30% (500-1000) of these neurons showed DETECTABLE activity on any given day, and not necessarily the same ones - there was a 50% overlap in the population- so any day, 1000 are active, and on another day, 500 will be the same as before and 500 will be new to that day - most cells (60%) showed activity on one or two days out of the ten- unique to that day - 20% of detectable each day were place cells |
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Describe the place cells in the track mouse running CA1 studdy. (3) |
- on average, a place cell (remember 20% of each day were determined place cells) only fired on 17% of the passes through that place - when place cells were identifies across more than one day, their place fields were identical- neither size nor location varied over time - there was a 15-25% overlap in the population of classified place cells from day to day.
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can we confidently determine where an animal was on one day just by the firing patterns of those cells and comparing them to the firing of other days? What is the process called? |
yes, because 25 or 20% of the place cells overlap each day, we are able to do this - this is called the Bayesian decoding technique - watch what cells fire, know which locations they correspond to . A month later you can use the cells to detect/predict where animal is - even with 15% overlap, a computer could still accurately predict locations. |
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each familiar area has a ______ in the CA1 |
-unique signature in the place cells via the 75%-80% of cells that do not overlap in coding ensembles from any two sessions - place cells that had a particularly stable and reliable place field on a given day were not likely be labelled as place cells in subsequent days in comparison with all place cells regardless of reliability |
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What does remembering an event entail (or what do we think it entails)? |
1) cortical sensory systems cause differentiating activity in the hippocampus grid and place cells. 2) later there is a partial cue which can come form cortex- outside event or internally generated. 3) These can restore the grid and place cell activiy in hippo to like it was when you first had experience, which then envokes the cortical sensory experiences (same areas imaging as experiencing) 4) Over time, and with repeated remembering, the memory becomes less dependent on the hippocampus, and the cortex is able to activate itself upon cues |
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Recall of recent memories vs old memories... why the difference in activation? |
recall of recent memories strongly activates the hippocampus, less the cortex recall of old memories strongly activates the cortex, less the hippocampus; a prominent theory is that the hippo is "training" the cortex so that it will be capable of retrieving memories on its own |
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What are the three models proposed for memory consolidation? |
First model proposed: Cortical Linkage
Second Model: Semantic Transformation
Third Model Proposed: Schema Modification - hippo is involved in updating the schema as you go through life - this way if you have a schema in place, learning is faster and more quickly hippo-independent |
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What is a schema? |
- a schema is an organization of related knowledge that contains semantic and episodic details, a mental structure of some aspect of the world - can have a self-schema, person-schema (traits of people in general), role schema (social positions in world), event schema |
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What impacts does sleep have on memory consolidation? (2) |
1) through sleep, episodic memories from the day prior should become more resistant to interference from new hippocampal learning the next day due to increased cortico-cortical connections formed during consolidation
2) after sleep, there should be a return of sparse encoding capacity within hippo, which restores the efficient ability for renewed next-day episodic. (the hippo fills up, and you need to sleep to stabilize what youve learned and clear the hippo to learn the next day) |
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Describt the studies on sleep deprivation (1) and napping (1) |
deprivation: sleep deprived 38 hrs then people asked to learn something
Napping: - when you first wake up from sleep , your ability to learn is at its peak. -**the amount of stage 2 non-REM sleep they had during the nap correlated positively with their learning ability later. |
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Explain the study showing how sleep protects against interference |
-give them a word pairs to memorize, would retest 12 hrs later - then in between the 12 hours they give them a second list with some of the words the same to confuse them. -Then have to recall the original pairs. - If you learn in morning then learn second pairs and recall all in one day you are bad, but if you learn the first list, sleep then learn the second, learning the second less interferes with your recall of the first |
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reactivation |
- this is what happens while you sleep - it happens across multiple sleep cycles, over many nights- gradual! - during oscillations, info gets passed from hippo to cortex - it strengthens neocortical connections that were initially weak, allowing them to eventually be largely independent - the hippo replays the info to slowly train the cortex to incorporate new info without disrupting the info that is already there - If you learn a bunch of new things (multi item) then can be incorporated during sleep into the “gist” or schema |
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Replay of place cells during sleep; sleep and selective remembering. |
- Place cells fire during sleep, seemingly walking through where the animal was that day. - If you play the animal tones like what they listened to during the day (to say go left or right for ex.) while they sleep, the associated neurons will activate while they are sleeping.;
- told to learn a list of words. -Told that some were important and some were not after learned. -Then tested on all words. -You remembered more of the ones you were told were important, and this effect is especially pronounced for the group that slept between learning and testing. - sleep more often promotes discarding neutral info as opposed to novel, emotional, rewarding, or explicit conscious instruction |
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Describe the study with the virtual maze |
- trained mice on a virtual maze, with head fixed, running on treadmill - after they sleep they get much better at the maze than if they dont- they can take shortcuts that they hadn’t taken before, and are confident in their turns. (staying awake leads to degradation) - sleep facilitates the extraction of a generalized spatial map of the maze from the complex episodic memories of the experience - not just sleep does this, although it preferentially happens during sleep, it may also happen at other “offline processing “ points throughout the day - when just chilling |
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How can a partial cue trigger a whole memory? what is this called? |
- In the CA3, every neuron is connected to every other neuron= auto-associative neural network - initially these connections aren’t strong enough to induce an action potential, but inducing synaptic plasticity here is very easy - so visual and auditory info come in, and both these neurons fire and they have a collateral which synapse on every other neuron, so they send collateral to each other, and they then become wired together - now when you just get maybe auditory and not visual, the two neurons are now connected, and activating one activates the rest. this is called PATTERN COMPLETION |
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What is pattern separation?
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- for pattern completion to be practical, memories must be stored far apart, other wise two memories encoded too similarly will converge onto a single, inappropriate memory
- output firing of the DG are less similar to one another then the input firing! - it tries to push the neural traces 'far apart' so that the new memory is distinct from old ones - it orthogonalizes the incoming sensory info |
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Give an ex of the kind of interference that pattern separation reduces and how the DG functioins
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- parking lot
- if I ask you what you did 3 days ago you would have a good idea but if i asked where you parked your car, less so - this is cue overload- the most effective retrieval cue is the one that is uniquely associated with a specific memory. The greater the number of associations a cue acquires, the less efficient it becomes at retrieving the desired memory - pattern separation helps to reduce this confuion |
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Describe info processing through the Entorhinal cortex and the DG
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Cortical input comes into the entorhinal cortex where it must go through grid cells before headline to DG and hippo. So between two dif classes, your grid cels in EC may be dif so the info may go through dif EC neurons to get to DG. But if you hear two tones in the same class you can distinguish them too even though grid cells are the same. They may go through the same EC but then be differentiated in the DG.
*There are many more neurons in DG than CA3 or EC. |
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Describe experimental ways to look at pattern separation and completion. What happens when we give a protein synthesis inhibitor?
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put animal in new room and shock him. Then next day put in slightly dif room, with some cues dif and some cues same. Animals that freeze upon entering the room have done pattern completion aka generalization. If they dont, they have had pattern separation aka discrimination
we can block the synaptic plasticity by blocking protein synthesis. If an animal has genralization and you give it a drug which destabilizes synapses, they no longer have the association to old room because when the neurons were active we disrupted the synapses. If they have discrimination, then giving them a synthesis blocker will disrupt the memory of the new room since the neurons from the old room weren’t active |
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What is Neurogenesis? Where can it happen?
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- the process by which neurons are generated from neural stem cells and progenitor cells
- most active during pre-natal development when it is responsible for populating the growing bring with neurons in mice, new neurons can form at the subgranular zone (part of DG) and the subventricular zone (lateral ventricles- ONLY IN MICE) |
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in adult humans, ___ new neurons are added to each hippo per day, = an annual turnover rate of __% of the neurons . How did they find this?
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700; 1.75%
- carbon labelling! -We know how much carbon 14 is in the atmosphere at any given timewhen you make a protein, carbon is taken from the atmosphere to use. the amount of carbon in that protein is set when it is made. But the radioactive carbon decays over a half life. This is how we do carbon dating. - We can do this in post mortem humans. Detected how much radio active carbon was in the neurons in their brain. all the neurons dated back to gestation in womb, except in the hippocampus. one third of the hippocampus (the DG) is eligible for turnover ad birth of new neurons. - when you are 90 years old, there is a very small percent of your original neurons left. |
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describe new DG neurons vs old ones. Natural stimuli activate...
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- highly excitable+ very plastic, while older neruons are hard to induce synaptic plasticity
- old neurons aid pattern separation, new neurons fire across multiple events - natural stimuli seem to preferentially activate adult-born (new) DG neurons (a higher proportion of new neruon expressed IEGs when a rat encountered new environment) |
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neurogenesis + depression; How long do most new neurons live? What influences this? (5)
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- Taking SSRIs seem to boost neurogenesis so people linked neurogenesis and depression but there is not direct connection...
- most new neurons dont incorporate successfully into the network and die in 2-3 weeks. This is effected by stress (decreases neurogen), exercise (increases neurogen) , age (decreases) , drugs (either or), new environment (complicated.. |
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What seems to affect neurogenesis?
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new learning events seem to influence neurogenesis in a complex manner such as by increasing and decreasing survival rates of new cells differentially according to age of the new cells and functional relevance
for ex. maze learning was shown to promote the survival of new nervous that were born 7 days earlier and at the same time apoptosis in new newtons that were born 3 days earlier. |
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Studies looking at neurogenesis and memory...
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have been inconsistent-
maybe due to different age, species, method of altering neurogenesis, task, time of learning and memory in relation to the neurogenesis manipulation |
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Modern theory on neurogenesis
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1) improved Pattern Separation: neurogenesis increases ability of hippo do form distinct memories of diff episodes- this is shown!
2) a possible downside is that learning improvement is accompanied by the forgetting of the older memories through the loss of info that was encoded by the old, removed neurons, so neurogenesis is the cause of forgetting... ** in other words, it aids pattern separation at the disadvantage of pattern completion (memory retrieval) |
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So specific interference= cue overload, but what is nonspecific interference mediated by? (2)
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1) any new learning- changes synaptic strengths in the hippo. will make old cues less effective and reproducing previous patterns of neural activity
2) neurogenesis: hippo is continuously evolving, so the likelihood that a retrieval cue will be able to reproduce a previous pattern of neural activity declines steadily over time |
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neurogenesis + age... (3)
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- neurogenesis declines with age- they labelled cells that underwent division, and there were less GFP cells in the older mice
- new neurons incorporate into existing network (labelled recently grown ones and new ones . New ones synapse right next to old ones and COMPETE) - adult mice have better memories than young mice (young mice dont fear a room they were shocked in as infants, and by two weeks dont remember it at all) |
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Immediate Shock Deficit
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- animals do not develop a room-associated fear if all the foot shocks come immediately upon being placed in the room
- contextual fear responses only develop if animals have time to explore a chamber for a couple unites before the aversive event occurs |
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describe the two studies on neurogenesis and exercise
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1) - marked cells undergoing apoptosis
- exercise reduces cell death in hippo - put mice in shock room, then one group given running wheel, one not - after a month the running wheel had more new neurons and didnt freeze as much when they returned to room - if you gave them 5 shocks, the memory was more salient, and less dif between two groups, but still - ** running first then learning doesnt affect later behaviour upon returning 2) put into water and have to swim. measure how long it takes them to find the secret platform. at baseline all animals learn it. Then one group runs for a month. after, they are worse at finding the platform that mice who didn’t run. |
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exercise does NOT impact....
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hippocampal - independent memories (like food poisoning) only hippo-dependent!
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Are exercise-induced changes in memory specifically related to neurogenesis? Giving them Memantine which boosts neurogenesis will...
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- try to prevent neurogenesis during the exercise period
1) nestin-cre transgenis mice *newly born neuons will express cre) 2) viral delivery of DNA into DG that encodes cre-dependent Thhymindine kinase 3) the drug ganciclovir kills all cells that express TK - running doubles the amount of neurogenesis in normal mice. If you block neurogenesis, animals dont forget after running! ->Memantine: This promotes forgetting! (as indicated by the return of the immediate shock deficit) taking them off drugs for two weeks doesn’t restore memory! you can kill the new neurons to stop the forgetting (with TMZ or other way) |
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Does Prozac promote forgetting?
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put mice on the barnes maze- a circle with a bunch of holes but one of the hoes is a compartment they can hide in.
-Mice will learn where it is. Give one group prozac, and they dont remember where the compartment is = pharmogologically-induced increases in neurogenesis also promote forgetting |
