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PHGY 314 > Brandon - Spatial Learning > Flashcards

Brandon - Spatial Learning Flashcards

1
Q

What is the story of the HM patient?

A

Scoville used to do frontal lobotomies to patients with schizophrenia and epilepsy

Once, Henry Molson walked in with the following problem: He had been hit by a bike and hit his head at 9yo → started having seizures (12/days)

They looked at his brain and saw the seizures originated from the uncus (hippocampus + amygdala-ish) → Scoville removed it

After the surgery, HM was fine and IQ was fine, but he couldn’t create new memories (old memories from before the surgery could be recalled)
He could also acquire new skills (ex: draw a star), but couldn’t remember learning them (the moment he was learning to draw the star)

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2
Q

What are the 2 types of long-term memory?

A

Declarative memory (explicit → hippocampus)

nondecralartive memory (implicit)

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3
Q

What are the different types of declarative memory?

A

Events (episodic memory)

Facts (semantic memory)

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4
Q

What are the different types of nondeclarative memory?

A

Procedural memory → skills (motor and cognitive)
Perceptual representation system → perceptual timing
Classcial conditioning → Conditioned responses between 2 stimuli
Nonassociative learning → Habituation sensitization

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5
Q

What are the main differences between the mouse and the human hippocampus?

A
  1. Human hippocampus ~ 100x larger than mice (and 10x larger than monkeys0
  2. They are in opposit orientations (human is a croissant facing up // mouse is croissant facing down/front)
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6
Q

What does hippocampus mean in latin?

A

Seahorse

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7
Q

What does CA stand for?

A

Cornu Amonis

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8
Q

How many cells and of what types are found in the dentate gyrus?

A
  • 1.2 million granule cells (excitatory)
  • 4K basket cells (inhibitory)
  • 32K hilar interneurons (20K mossy cells) (inhibitory)
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9
Q

How many pyramidal cells are found in CA3 and in CA1?

A

330K pyramidal cells in CA3
420K pyramidal cells in CA1
+ various interneurons (inhibitory)

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10
Q

How many cells are found in layer II of the entorhinal cortex?
How many cells are found in the subiculum?

A

Entorhinal Cortex:
~ 200K cells (mostly pyramidal)
~ 20% interneurons?
Subiculum:
~ 180K pyramidal cells

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11
Q

What are the different projections of the entorhinal cortex onto the hippocampal areas?

A

Layer II of EC → DG/CA3
Layer III of EC → CA1/Subiculum
CA & Subiculum → back to EC layer V

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12
Q

What are the main circuits of the entorhinal-hippocampal system?

A

Direct pathway:
EC layer III → CA1

Indirect pathway:
EC → DG → {mossy fibers} → CA3 → {Schaffer collaterals} → CA1

*CA3 has lots of recurrent collaterals onto itself
*Mossy fiber synapse is one of the largest and most powerul synapses in the brain

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13
Q

How many projection onto DG from the perforant path?

A

~ 4500 spines/granule cells (75% from EC)
- 1 EC cell makes ~ 18,000 synpases with granule cells (in DG)

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14
Q

Where can CA3 receive its inputs from?

A

50-80 mossy fibers from DG

3,500 perforant path synapses from EC II

12,000 recurrent collaterals from other CA3 cells (majority)
- 8,000 to basilar dendrites (stratum oriens)
- 4,000 to apical dendrites (stratum radiatum)

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15
Q

Where do CA1 inputs come from?

A
  • From CA3 Schaffer collaterals: 4,500 basilar; 6,500 apical synapses
  • From EC layer III: 2,500 synpases

*CA1 proximal to DG receives medial and distal inputs from DG

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16
Q

What are the 2 areas of the entorhinal cortex?

A

*Area are no the same as layer (both layers II and III are found in both areas)

Lateral Entorhinal Area → layer II projects to distal dendrites on DG and CA3

Medial Entorhinal Area → layer II projects to intermediate dendrites on DG and CA3

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17
Q

What are the 3 major fiber systems of the hippocampus?

A
  1. Angular bundle from EC → perforant path (and more)
  2. Fimbria/fornix to subcortical areas (mostly cortical input from the medial spetum)
  3. Dorsal and ventral commissures link hippocampi
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18
Q

What is the difference between dendritic arborization of principal (pyramidal) cells vs granule cells

A

Pyramindal cells → bipolar dendrites (basal and apical/both sides of the sooma)

Granule cells → unipolar dendrites (sooma is in the DG infra/supra-pyramidal blade and dendrites project to outside)

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19
Q

What are the different layers of CA1?

A

Apical → Basal (deepest)

  1. Stratum lacunosum-moleculare → entorhinal afferents
  2. Stratum radiatum → Schaeffer collaterals
  3. Stratum pyramidale (pyramidal cell soomas)
  4. Stratum oriens (basal dendrites go that way)
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20
Q

What are the different layers of the CA3?

A

Apical → basal
(0. Stratum Lacunosum moleculare)
1. Stratum radiatum: entorhinal afferents, mossy fibers enter from DG
- Stratum radiatum makes synapses in stratum lucidum
2. Stratum lucidum (large spines coming from mossy fibers)
3. Stratum pyramidale (pyramidal cell soomas)
4. Stratum oriens: recurrent collaterals

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21
Q

What did the Morris water maze experiment show?

A

Memory is impaired by inactivation of the medial septum or by lesions in the hippocampus
- Specifically lesions in the dorsal hippocampus

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22
Q

How did they study the fact that the hippocampus encodes recent memory specifically?

A
  1. Put rat in a new environment (box with shock grid on the floor) → context fear conditioning
  2. Lesion the hippocampus (of SHAM) 1, 7, 14, 28-days post-context fear conditioning
  3. Asses if the mouse freezes (remembers) or not when put back into the box

Results:
For lesions 1, 7 and 14 days post-conditioning, the mouse didn’t remember (freeze)
For lesions 28 days and after, the mouse remebered (froze)
Conclusion → it takes about 28 days for information to go from hippocampus to the cortex and become long term memory

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23
Q

Where in the cortex are found important neurons for location of the animal?
Which are these cells?

A

Neurons in the medial temporal lobe → Medial EC, presubiculum, Hippocampus

Grid cells, Head direction cells, Place cells

*Recorded extracellular very close to the neuron to assess spiking with electrodes

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24
Q

How where Lavilleon et al, able to show that place cells are maintained and associated with navigation?

A
  1. Target 1 place cell which is stimulated in a specific region of a given open field
  2. With a Medial forebrain stimulation (dopaminergic fiber), reward the animal everytime that cell fires
  3. Take the animal out of the environment
  4. The next day, put the animal back → it will run to the location in the field that stimulates this place cell

Do the same but give reward during sleep when that place cell fires spontaneously → the next day, the mouse will still run to the location that activates this place cell

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25
Q

Which cells are considered to act as our internal compass?
What are an important feature of them?

A

Head direction cells
They are hard-coded, not experience based → pups had them in P11 pups (pups open their eyes for the first time at P8-9)
*Recorded in the Pre-subiculum and para-subiculum of the pups

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26
Q

What is the general plan of the brain circuit involved in generating the head direction cells, Place cells and Grid cells signal?

A
  1. Vestibular system has Angular Velocity cells (AHV)
  2. Lateral Mammillary nucleus (LMN) = AHV cells and HD cells (head direction)

LMN → ADN (Anterodorsal thalamic nucleus) → Pre/post-Subiculum → Entorhinal cortex → Hippocampus

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27
Q

The interaction between which 2 nuclei is critical for generating head direction cell signal?

A

DTN (Dorsal tegmental nucleus in vestibular system → AHV cell)

LMN (Lateral mammillary nucleus → AHV and HD cells)

Evidence:
1. Lesion in DTN imparis ADN HD cells
2. Lesion of LMN impairs ADN HD cells
3. Lesion of ADN impairs postsubiculum HD cells
4. Lesion of postsubiculum does NOT imapir ADN HD cells
*Hierarchy from vestibular → thalamus → cortex/hippocampus (require input for the lower areas)

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28
Q

Which type of cells are found in the DTN? LMN? ADN? pre/post-subiculum? Entorhinal cortex? Hippocampus?

A
  1. Dorsal tegmental nucleus → angular velocity cells
  2. Lateral mammilary nucleus → mostly head direction cells (maybe a bit of Angular velocity cells)
  3. Anterodorsal thalamic nucleus → head direction cells
  4. Post/pre-subiculum → head direction cells
  5. Entorhinal cortex → head direction cells, grid cells, place cells
  6. Hippocampus → place cells
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29
Q

What is the tuning curve life for LMN vs ADN vs postsubiculum?

A

LMN → broad tuning curve (~180˚)
ADN (Anterodorsal thalamic nucleus) → more narrow tuning curve
Postsubiculum → even more narrow

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30
Q

What makes head direction of the ADN different?

A

They exhibit “anticipatory” firing

The peak is a bit shifted dependent on wether the mous is turning CW or CCW anticipating the future head direction → postsubiculum neurons, when they get the input, they correspond exactly to the direction of the head

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31
Q

What do head direction cells on the AND depend on?
What experiment demonstrated this?

A

They depend on vestibular inputs

Lesions hair cells from the vestibular system with Sodium arsanilate (into inner-ear) → ne more response/firing form the HD cell of ADN

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32
Q

What experiment was done to confirm head direction cells where actually responsible for our internal compass?

A
  1. Mouse starts in a little refuge and is let free in a completely dark room
  2. It encounters a large food pellet
    - Natural instinct is to bring the large food pellet back/run with it
  3. The mouse runs back to the refuge → slight error in spatial navigation, the mouse gets close, but not straight to the refuge

Compair this error with the shift in the head direction cells tuning
- In the dark, HD cell tend to shift a bit creating an error in comparison to the environment

They did show that the error in returning angle to the refuge correlated to the shift in head direction cells

33
Q

They tried to assess head direction cell activity in a 3D environment with rats. How did they do it and what was their results?

A

Put mouse in a box where can climb everywhere. Start on 1 side and want to get to food on the other side, but they have to climb by the ceiling to access it because the direct floor path is blocked.

When climb the walls → head direction cells fire as if it was a continuation of the floor
On the ceiling → head direction cells stop firing
*Not great study model because rats don’t live in 3D

34
Q

What animal model did they use to assess head direction encoded in 3D?

A

Used wireless recordings on bats.

2 hypotheses:
- Spehrical coordinates
- Toroidal coordinates (actual case)

35
Q

What model corresponded to the 3D coding of head direction cells in flying bats?

A

Toroidal coordinates:
- Azimuth cells → only care about the azimuth no matter the pitch
- Pitch cells → only care about the pitch no matter the azimuth
- Azimuth x Pitch cells

36
Q

What was found about head direction cells during sleep?

A

They replay different direction of the head (sets of neurons related to different directions are activated → seen by decoder)

Slow wave Sleep → lots of head direction motion
REM → slow rotation in head direction (according to the sets of neurons firing)

37
Q

How do place cells of the hippocampus encode 3D space in rats vs bats?

A

Put rats on a spherical stair case → no notion of Z-axis, the same X-Y place cells fires at every turn of the plateform at the same location

Bats have X-Y-Z place cells

38
Q

What is an attractor state?

A

An attractor state is a set of neurons that fire corresponding to a specific object/ location

Ex: in the duck/rabbit illusion, we either fall into the duct attractor state or the rabbit attractor state → takes energy to switch from one to the other

39
Q

What is pattern completion vs pattern separation?

A

Pattern completion = when stuck into 1 attractor state, even when noise is added/input changes a bit, the output stays the same (see the same thing)

Pattern separation = When the input changes too much, the output also changes → change attractor state

40
Q

What is the difference between global remapping and rate remapping?

A

*Hippocampal CA1 place cells
Global remapping:
A place cell fires in very different location in 2 different rooms/fires in one room, but does not fire in the other room
- For very different rooms
*Change attractor state → associated with pattern separation

Rate remapping:
A place cell fires in the same location in 2 rooms, but at different rates
- For same room, but change wall color for example
*Stay in the same attractor state (same subset of cells firing) → associated with pattern completion

41
Q

How do hippocampal place cells signal memory?

A

They do so by changing their firing rates

T-mase where the mouse goes right, then left, then right, then left and gets food at start point if he does it good
→ Place cells fire more/less depending on if the animal has to go right or left (shows memory form 30 seconds ago)

42
Q

Could CA1 still produce place fields when CA3 was lesioned?

A

Yes
CA1 place field formation is not dependent on Schaffer collaterals coming from CA3

43
Q

Which cells are considered to be the main input onto CA1 for generation of place fields?

A

Grid cells from the Medial Entorhinal Cortex, through the Layer III perforant path
*Mostly dorsal MEC (ventral MEC have weaker spatial tuning)

44
Q

What is the difference betwee grid fields in a very small envrionment and in a large envrionment?

A

Small envrionment → place fields take a bigger portion of the envrionment/appear bigger

Larger envrionment → more firing spots, can better the see the grid pattern

45
Q

What are important features of grid cells?

A

Grid pattern:
- Hexagonal grid of fields
- From the center → ~60˚ shifted lines of firing spots → equilateral triangles
- Gird cells fire in complete darkness (following the internal compass, don’t require visual input)
- All grid cells fire in all environments
- Immediately formed in new environments and evolve/get more complete as you navigate it

46
Q

How did they find evidences for grid cells in humans?

A

Can’t really record from the MEC in humans → measured Blood flow/glucose around the grid cells?

As grid cells have shifted lines of firing spots every 60˚, make the person move in a virtual environment and shift direction a bit → every 60˚ they an increase the BOLD activity

47
Q

How can grid cells induce global remapping of CA1 place cells?

A

Entorhinal grid cell realign (shift in the place fields) → global remapping

48
Q

How do grid cells place fields change from dorsal to ventral medial entorhinal cortex?
How does this reflect in the hippocampus?

A

Dorsal → more numerous smaller place fields
*Progressive increase
Ventral → fewer larger place fields, more spaced out

*Observed by making mice run on a linear track and recording form different areas

Hippocampus:
Dorsal → more narrow place field
Ventral → larger place field (even up to 10m diameter)

49
Q

How do grid cell adapt to multi-compartmental envrionments?
Ex: Hair-pin maze

A

Grid cells encode each hallway very similarly as if they where the same envrionment (1 out of 2 because the go north, come back south, then north, etc.)
→ Fragmentation of grid cells

*Hippocampal place cells do the same thing

50
Q

What was seen in the experiment in which they lesioned the medial septum?

A

Lesion in the medial septum → no input onto Medial Entorhinal Cortex (can still fire, but no grid cell spatial firing pattern)
*Eliminates theta oscillations throughout the medial temporal lobe

Then they tested CA1 place cells in a familiar and novel envrionement:
→ CA1 place cells were suprisingly able to develop new place fields in a novel room without septal inputs and without grid cells
→ They also conserved the place fields in familiar rooms

Hypothesis: different cell types in the medial entorhinal cortex can drive formation of place fields, not only grid cells

51
Q

What are the different cells found in the MEC?

A
  1. Grid cells → no directional tuning
  2. Head direction cells
  3. Conjunctive cells → grid patterns + head direction tuned
  4. Boundary vector cells → create large field that spans 1 axis of the envrionment and codes for distances from the boundaries of the envrionment
  5. Speed cells → firing rate of thses cells is linearly correlated with runing speed
52
Q

What other cells from MEC than grid cells could possibly drive the generation of place cells in CA1?

A

Boundary vector cells

2 or more boundary vector cells → input together → Place cells to fire in a specific location

*Not affected by medial septum inactivation/lesion
~20% of MEC = grid cells
~2% of MEC = boundary vector cells

53
Q

Which cells can encode for the When component of episodic memory?

A

Time cells

Experiment:
1. Have a rat run for 15secs on a treadmill
2. Door opens
3. Alternating T-maze task
4. Repeat

Lots of cells firing in the 1st second, but different cells firing after 2, 3, 4, 5… seconds

Grid cells can code for distance and time of the treadmill task, some will fire only at 1 place/time, some will fire every 3 seconds, etc.

54
Q

What are hippocampal theta oscillations?

A
  • Largest oscillations in the mammalian brain
  • 6-10 Hz (relatively slow) oscillations in local field potential in the hippocampus and related structures
  • Observed during exploratory and attentive behaviours
  • Seen in rats, mice, gerbils, rabbits, bats, pigeons, monkets, humans
  • Reflect highly and precise spike timing throughout the hippocampal structures

*every 125ms ~ 8Hz

55
Q

What is Theta phase precession?

A

It is a caused single unit acceleration of the spiking activity of a neurons when the animal enters its place field
Seen when animals ran on a linear track:
- At the start of the place field, firing at the peak of theta oscillation
- Slowly shifts at the neurons has a slight increase in firing rate (~10Hz instead of 8Hz for ex)
- At the middle point of the place field, the neuron fires in the bottom of theta local field oscillation
- At the end of place field (location), firing has shifted back to the peak of the theta oscillation
- When exit the place field, the neuron’s firing rate falls back into the theta oscillation rhythm it was following before the animal entered it place field

*Correlation (negative slope) in the delay between peak or theta oscillation and firing CA1 place cell and where the animal is in the place field
*When walking, shift slower than when running as advance slower in the the place field

56
Q

Where is phase precession observed?

A

*Occurs when the animal is in exploratory, attentive behaviour

  • In entorhinal layer II Grid cells
  • CA1 place cells
  • NOT entorhinal layer III grid cells → phase locked, meaning they only fire following the theta oscillations regardless of position on the track
57
Q

What is phase precession the result of?
What experiment showed this?

A

Phase precession is the result of the neuron oscillating faster than the extracellularly recorded theta oscillation

Did so by comparing extracellular field and intracellular recordings:
- Fix head of mouse so it can’t move (for intracellular recording)
- Body can still move and is on a ball
- When the mouse runs on the ball, it navigates in this virutal world in front of it

58
Q

What is the consequence of phase precession?

A

Precise temporally structured cell assemblies

Different place cells which have neighbouring place fields are just a bit delayed creating an order of their sequence of activation
- When the animal enters a new place field, that cell starts firing with theta oscillations, then under goes phase precession and comes back to theta rhythm at the end of the place field

Halfway through the track, the hippocampus has a redout of the the place fields from the start of the track to the end of the track within 125ms (1 theta oscilation) as they are all closely delayed in sequence of activation

59
Q

What are Sharp-wave ripple?

A

Sharpe-wave ripples are events that occur in non-theta states, when the animal is still (when there are no theta oscillations)
These Sharp-wave ripple events propagate throughout the hippocampal formation (CA1, CA3, Subiculum, EC, Parasubiculum, etc.)
- Activation of pyramidal cells
*Occurs during slow wave sleep and daydreaming/resting, conserved across species (not REM sleep or exploration/attention/running)

Sharp-wave = 1 slow, but very large deflection of 1-50Hz / ~2mV

Ripple = many quick oscillations on top of the sharp-wave (1Hz - 10kHz, ~ 0.5mV)

→ Sharp-wave ripples trigger activity throughout ALL of cortex (not subcortical areas, done by FMRI bold signal recording)

60
Q

When an animal run on a linear track, what is the sequence of place cell activities recorded before, during and after?

A

Before → Shortwave ripple event activating all place cells that will be activated during the run in the sequence they will be activated (Pre-play)

During the run → Place cells are activated and undergo phase-precession in order of place fields

After the run → Sharpwave ripple event activating the place cells, but in reverse order (Replay backwards)

*During sharpwave ripples, there is decoding of the position of the animal (place cells fire as if the animal was in a specific location, but the animal is resting not at that location)

61
Q

How did they show that blocking hippocampal sharwave ripples impaires memory consolidation?

A

Setup:
1. Put a mouse in the middle with 6 linear tracks (forming a star)
2. Put food baits at the end of 3 of these tracks
By the end of the day, the animal knows which tracks have the food

  1. Allow the animal to rest for 1 hour outside the task envrionment
    During this hour:
    - Control group → After each sharpwave ripple event, silence neuronal activity for a short period
    - Experimental group → At the start of each sharpwave ripple event, silence neuronal activity for a short period (no replaying/ripple events for memory consolidation)
  2. Redo the task → experimentl group has worse results than control group who did have consolidation through shortwave ripple events (replaying)

To silence neuronal activity, they stimulated the commissure pathway connecting right CA3 to left CA3 → causes almost all hippocampal neurons to fire at once → causes a general synchronized refractory period of 200-300ms

62
Q

What are hippocampal gamma oscillations?

A
  • 30-100 Hz oscillations in local field potential in hippocampus and related structures
  • Co-occur with hippocampal theta oscillations
  • Thought to function to coordinate activity between distant structures
  • Seen in rats, mice, gerbils, rabbits, bats, pigeons, monkeys, humans

Experiment showed that hippocampal gamma oscillations increase prior to choice point on an alternation taks:
- Circular alternating T-maze with delayed section (treadmill)
- Gamma oscillations were weak when animal was coming back to the delay zone
- Increased in power as the animal was approaching the point of decision of the T-maze → where it had to retreive information from memory (what did it do last time?)

63
Q

What are slow and fast gamma oscillation of CA1 synchronized with?

A

Slow (~40Hz) gamma reflects CA3-CA1 synchrony

Fast (~90 Hz) gamma reflects MEC-CA1 synchrony

*All regular within the theta oscillations

64
Q

What experiment showed Gamma coherence between LEC and distal CA1?

A

Setup:
Animals exposed to odor cube → if given odor A, have to go to food pellet A, if given odor B, have to go to food pellet B
- LEC is though to be responsible for odor processing
- Animals learned the task for 5 days

There was Gamma coherence between LEC and distal CA1 supporting the associational learning:
- LEC and dCA1 are connected (need to be connected to an area to have coherence, MEC is connected to proximalCA1)
- At day 1, weak coherence between LEC and dCA1
- At day 5, much stronger coherence between LEC and dCA1 + much better performance at the task
- In the failed trials at day 5, decreased coherence between LEC and dCA1 for that specific trial was observed (shows coherence is required)

65
Q

How do different attractors compete with each other at the network level in discrete attractor network?

A
  1. Sensory input stimulates 1 neuron af attractor A
  2. Neuron A spreads the signal to the other neurons of attractor A (excitatory connections)
  3. Neurons from attractor A send inhibitory signal to all other attractors (neurons) → Feedforward inhibition

Compeition / selection of attractor networks

66
Q

How do different attractors compete with each other at the network level in continuous attractor network?
What is the best example of a continous variable in this case?

A

Continuous attractors → head direction
*Signal is generated at the lebels of Dorsal tegmental nucleus (DTN) → Lateral Mamillary nucleus (LMN)

Attractor model requires recurrent excitation + lateral inhibition:
- Connections are organized in a ring
- When facing north → sensory input activates the neuron “at the north of the ring”
- This neurons sends excitatory input to neighbouring neurons → recurrent excitation
- This neuron sends inhibitory input to neurons farther in the ring

This allows maintenance of the signal (by recurrence) as neurons operate on a much faster time scale as perception

67
Q

Which animal actually showed a ring attractor for head direction?

A

Drosophila had a ring of neurons coding for head direction
Experimental setup → fixed head, free body on a spining ball, the drosophila looks at a screen with a LED
- Look at deconded position of animal (ring signal) vs LED

68
Q

How does the attractor model apply to grid cells?

A

In grid cells, every neuron, when activated, will send excitatory signal to its neighbouring neurons and inhibitory signal to neurons farther in the field
→ Easy to produce place cells form this system

For grid cells, neurons that are connected by excitatory input → theoretically close if you fold the space field (neurons of the EC and their place fields) into a doughnut shape → close neurons in the doughnut form excitatory connections

69
Q

Which cells code for distance and time on the treadmill task?
What is the name of the model explaining this situation?

A

Grid cells
Oscillary interference model → generates time cell firing

70
Q

What model do grid cells follow which explains time cell firing?
What data was shown to support this model?

A

Model → Oscillatory interference model
1. Intrinsic frequency (from dendrites/sensory input, faster~9Hz)
2. Network frequency (from sooma ~ 8Hz → theta oscillation rhytm)
Sum up → When out of phase ~ 0 amplitude, When in phase ~ Large amplitude
- Set a threshold for spiking → Spiking pattern of regular bursts based on the sum of these frequencies
*Requires both rhythms to be constant

By inactivating the medial septum (supporting the network frequency of hippocampal theta oscillation) → no summing → loss of the timing properties
Thiming cell need theta oscillations

71
Q

What do timing cells absolutely require?

A

Theta oscillation (supported by medial septum) → for summing with the intrinsic frequency

72
Q

How is the oscillatory interference model used to stimulate grid cells?

A

Sum up these different frequencies:
1. Baseline theta (sooma)
2. Input from different head direction cells trough dendrites at different frequencies (can have many different frequencies)

When all signal are enough in phase for the sum to surpass the threshold → spiking

This spiking pattern/sufficient sum will occur in different locations in the RF creating a grid pattern

73
Q

What explains the progressive increase in grid scale from dorsal to ventral medial entorhinal cortex at the network level?

A

*From the oscillatory interference model
There is a gradual increase of grid scale along dorsal/ventral axis → Correlates with an decrease in intrinsic frequency of MEC neurons along dorsal/ventral axis

Dorsal → smaller grid scale → higher intrinsic frequency → more often, but shorter period over spiking threshold

Ventral → larger grid scale → lower intrinsic frequency → longer periods over the threshold, but less often

74
Q

What are hippocampal theta oscillation important for in memory?

A

Encoding and Retrieval:
Theta rhythm modulation of LTP for encoding dynamic

EC → LTP onto CA1, but also prefer to fire at the peak of theta wave
CA3 → LTD onto CA1, but also prefer to fire at the trough of theta wave

75
Q

What conditions are prefered for encoding in the hippocampus vs retrieval?

A

Theta wave dictate encoding vs retrieval patterns and separates them in time (different phases of the wave).

Encoding:
- Peak of theta wave
- Strong EC input (→ CA1 and CA3), weak CA3 input onto CA1
- Strong LTP

Retrieval:
- Through of theta wave
- Weak EC input, Strong CA3 input (→ CA3 (recurrent) and CA1)
- LTD/depotentiation

76
Q

What happens at the level of the hippocampus when we have a déjà-vu?

A

When encoding of a new memory and retrieving of an old memory occur at the same time in the hippocampus → CA1
*They normally should occur at different phases of theta oscillations

77
Q

How do ACh level in the neocortex and in the hippocampus affect encoding and retrival or memory?
When are they higher vs lower?

A

ACh highest when walking/active and lowest in Slow wave sleep (medium when resting awake)

Cholinergic presynaptic inhibition of glutamate release in cortical structures (hippocampus, olfactory, EC)

High ACh: Strong input from EC → CA1 (encoding), but inhibited feedback within the hippocampus (retrieval)
*Neocortex → Hippocampus

Low ACh: Weaker input from EC → CA1 (encoding), but strong feedback from CA3 (retrieval/consolidation)
*Hippocampus → Neocortex

78
Q

What is the effect of stimulation of cholinergic inputs to hippocampus on sharp wave ripples?

A

It block sharp wave ripples

*Medial Septum stimulation → responsible for cholinergic input onto the hippocampus → blocks sharpwave ripples
- Correlates with less consolidation and more encoding
- When low ACh, more sharp wave ripples and more consolidation/retrieval

79
Q

What is the 2 stage model of memory consolidation?

A
  1. Local effect of ACh in the hippocapus blocking reafferent inputs during active state/encoding
  2. Theta oscillations vs Sharp wave ripples

PHGY 314 (8 decks)

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