Lecture 4 & 5 Questions Flashcards

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1
Q
THE HIPPOCAMPUS
what is the particular function of each subdivision of the hippocampus:
- dentate gyrus
- CA3
- CA1 cell groups
A
  • dentate gyrus: processes space and time
  • CA3: does the encoding, retrieving, pairing, comparing of new stimuli with LTM; and pattern completion
  • CA1: LTM for space and temporal ordering; communicates with cortex for remote memory storage
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2
Q

NEURAL PATHWAYS
understand the distinction between the sources of input and types of information transmitted to the hippocampus from the:
1. lateral entorhinal cortex
2. medial entorhinal cortex

A
  1. lateral entorhinal cortex
    - content
    - local
    - items and events
    - what is out there
    - where is it
  2. medial entorhinal cortex
    - context
    - global
    - spatial framework
    - where am i
    - where am i going
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3
Q

RHINAL PATHWAYS
discuss the differences in how information flows between the entorhinal cortex and CA1 under:
1) normal conditions
2) when learning occurs because of salient/important stimuli

use the following terms to describe these interactions:

  • LRIP (long range inhibitory projections
  • CCK (cholecytstokinin)
  • FFI (feed forward inhibition)
  • ITDP (input timing-dependent plasticity)
  • significance in the order of inputs from the EC and CA3 in exciting CA1 to produce ITDP
A

Under Normal Conditions
(2) Information from the Lateral Entorhinal Cortex (LEC) would travel to the Dentate Gyrus then to the CA3 (via mossyfibers) and then to the CA1 (via schaffer colateral). Along with being sent directly to the CA1, information from the CA3 will activate cholecystokinin (CCK) which will excited the Feed Forward Inhibition (FFI). This process will INHIBIT information from exciting the CA1. So the other information that was sent to the CA1 from the CA3 is nullified.

Under Salient Conditions
(1) Information from the LEC is sent via the Long Range Inhibitory Projections (LRIP) from the Entorhinal Cortex (EC) will inhibit the CCK area before the signal from CA3 arrives to excite it. Because the CCK is inhibited, the FFI is also inhibited, which means the inhibitor can’t do its job of inhibiting, aka it has been disinhibited. Because the FFI is disinhibited, the LRIP sends direct ED projections to CA1 that are excited by the event.

(3) Information from the LEC is also sent directly from the EC without going through any other process. Normally, this step would not be enough to activate the CA1, but because the previous step just happened, it adds to the overall effect of the CA1 activating.

Input Timing Dependent Plasticity: all of that can only happen because the (1) happens 20 seconds before (2) and (3)

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4
Q

LONG TERM POTENTIATION

how is ltp defined and how does this definition parallel it to describe learning?

A

LTP: long lasting changes in the responsiveness of neurons are created as a result of previous experience with high intensity or high frequency stimulation

LTP and learning
- associativity

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5
Q

LONG TERM POTENTIATION
describe the sequence of chemical changes that lead to potentiation at the synapse
(glutamate binding to AMPA receptors, depolarization, expulsion of magnesium from NMDA receptors, calcium entry, etc.)

A
  1. strong stimulation
  2. glutamate is released
  3. glu binds to ampa receptors which opens up ampa for business
  4. ampa’s being open allow for na2 to flow out, depolarizing the cell (-70 to -55)
  5. nmda receptors are normally blocked by mg2 but because of the depolarization, they are released which opens nmda up for business
  6. ca2 flows into nmda receptors which are important for catalyzing the LTP processes
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6
Q

LONG TERM POTENTIATION

know the significance of NMDA receptors in serving as “coincidence detectors”

A

the activation of nmda receptors tags/marks which pre & post synaptic neurons are active at the same time

  • tagged via proteins
  • because X was happening while Y was going on, that must mean that X and Y are related
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7
Q

LONG TERM POTENTIATION
understand the sequence of intra-cellular events (6) that are initiated by calcium entry through NMDA receptor

understand how these changes lead to the development of proteins

A
  1. Calcium entry
  2. Activate cAMP
  3. Activate kinases
  4. Phosphorylate proteins (CREB)
  5. Transcribe new genes
  6. Develop new receptor proteins
    {7. Tag or insert new receptor proteins}
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8
Q

LONG TERM POTENTIATION

what is the significance of the new proteins in the process of “tagging” receptors that are active at the same time?

A

They create associations between events

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9
Q

LONG TERM POTENTIATION
how are the components of Hebb’s cell assembly model related to the processes that actually occur during LTP to bind new information into a memory trace

A

Associativity: Inputs active or firing at the same time become associated or wired together so that the response produced by one will also be produced by the other

  • active synapses are tagged
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10
Q

CALCIUM
Describe how Calcium entry through NMDA receptors result in the following:
a) increased glutamate release from the presynaptic axon
b) increased insertion of AMPA receptors into the postsynaptic dendritic membrane

A

Increased glutamate

  1. Ca2+ activates nitric oxide
  2. NO acts as a retrograde messenger
  3. NO affects the PRESYNAPTIC vesicle
  4. More glutamate is released

The heightened response to glutamate is the potentiation

Increased insertion of ampa
1. CamKII initiates the process to insert additional ampa receptors in the dendritic shaft

Resulting in structural changes between pre and post, as well as creating a heightened response to glutamate and adding a greater level of potentiation

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11
Q

CALCIUM
How does the CaMKII activity regulate AMPA (i.e. GluR1 receptors) activity
Understand the interactions of CaMKII with PKA and PKC and their specific actions on
Serines 818, 831 and 845.

A

2 stages of trafficking ampa glu receptors to dendritic spines

  1. PKA (step 1) phosphorylates P3 (ser 845 site) which translocates the unit to the extra synaptic region
  2. Ca2 (step 2) influx via NMDA receptors activates PKC (step 3) and PKC phosphorylates P1 (ser 818) which transports receptors to post synaptic density zone

Step 1: PKA Ser 845 traffics GLU to extra synaptic region
Step 2: CamKII Ser 831 changes GLU’s channel conductance
Step 3: PKC Ser 818 anchors GLU to PSDZ

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