Learning And Memory I & Ii

Front 1

What is the definition of synaptic plasticity?

Back 1

The ability to change the strength of The synaptic connection between neurons

OR the ability to change how much depolarization is caused by a single synapse firing

Front 2

What are some modes in which there is a lasting increase in presynaptic NT release in response to an AP? (4)

Back 2

1. Increased NT in each vesicle
2. Increased number of vesicles
3. Decreased uptake (glutamate) or breakdown (Ach) of released NT
4. Increased Ca into presynaptic terminal

Front 3

What are some ways in which there is a lasting increase in postsynaptic receptor responses? (2)

Back 3

1. Phosphorylation of receptors --> increase amount of current flow or time the channel is open

2. Insert more receptors

Front 4

How can alterations of the structure of a synapse increase the strength of the synapse?

Back 4

Increase the area of synaptic contact

Front 5

How can altering the number of synaptic connections between neurons increase the synaptic strength?

Back 5

1. Grow new synapses between neurons
2. Splitting of a single synapse into 2 synapses

Front 6

What is 'use dependent synaptic plasticity'?

Back 6

Strength of synapse is changed as a result of specific patterns of neuronal/synaptic activity

Front 7

What is the time scale of facilitation?

What is another name for facilitation and why?

Back 7

milliseconds

Paired-pulse diffusion because 2 presynaptic stimuli given within 10-100 ms of each other --> larger second response

Front 8

What is the mechanism of facilitation?

Back 8

AP --> Ca influx to presynaptic terminal --> another AP before all the Ca is cleared --> more NT released because more Ca

Front 9

What is the time scale of Depression?

Back 9

milliseconds --> seconds

Front 10

What is the mechanism of Depression?

How does recovery take place?

Back 10

Depletion of readily releasable pool of synaptic vesicles with repeated high frequency stimulation

Recovery = new synaptic vesicles recruited to release

Front 11

What is the time course for Post-tetanic potentiation (PTP)?

Back 11

Minutes; onset can be delayed after a high frequency, presynaptic activation

Front 12

What is the mechanism of PTP?

What is this reaction a response to?

Back 12

Ca-dependent biochemical process that induces increased NT release lasting up to several minutes

Response to brief, high frequency "tetanic" stimulation

Front 13

How is PTP different that PPF?

Back 13

PPF = residual Ca causes increase in NT release

PTP = biochemcial change in release machinery from increased Ca leads to increased NT release; PTP lasts longer than PPF

Front 14

What is Hebb's Postulate?

Back 14

If cell A repeatedly/persistently excites cell B, the strength of the synapse between A and B increases

Front 15

What is long-term potentiation?

Back 15

Brief, high frequency, "tetanic" stimulation of presynaptic neurons --> increase size of the synaptic response over the long term

Front 16

What is anterograde memory loss?

Back 16

Inability to learn new information, but able to remember old

Front 17

What are the functions of the hippocampus?

Back 17

Encodes temporal relations between events, spatial memories, and other types of memories

Front 18

From where is the hippocampal input?

How is information transferred through the hippocampus?

Back 18

Input from the entorhinal cortex via the perforant path axons

Transferred via the trisynaptic circuit

Front 19

What is the major hippocampal output?

Back 19

CA1 pyramidal neurons

Front 20

What is the order of the trisynaptic circuit?

Back 20

1. input --> Perforant path axons (entorhinal cortex) --> granule cells of dentate gyrus

2. Granule cells send mossy fibers (axons) --> CA3 pyramidal cells

3. CA3 pyramidal cells send Schaffer collaterals (axons) --> CA1 pyramidal cells --> output

Front 21

What happens to the response of a CA1 pyramidal cell (postsynaptic) when the CA3 pyramidal cell (presynaptic) is stimulated with high intensity?

Back 21

Postsynaptic response is much higher than normal, even when reintroduced to a low-intensity stimulus again

Stays that way for hours

Front 22

What does it mean that the LTP is a use-dependent form of long-lasting synaptic plasticity?

Back 22

Using a synaptic connection in a certain, strong manner leads to a long-lasting change in the strength of the synaptic connection

Front 23

What does it mean that the LTP is input specific?

Back 23

LTP increases are specific to the synapses that were activated during the high frequency stimulation

Front 24

What is associativity?

Back 24

Association of a weak input on one pathway and a strong input on another leads to long-lasting increase in strength of the weak input (LTP)

Front 25

How does the associativity of LTP explain associative learning? (Pavlov's dog)

Back 25

Strong stimulus = food
Weak stimulus = bell

When bell alone --> no salivation
When bell with food --> salivation
Over time, bell alone --> salivation

Front 26

What are the two requirements for associativity?

How does this explain how associativity works?

Back 26

LTP needs
1. Presynaptic activation
2. Strong postsynaptic depolarization

STRONG input provides the postsynaptic depolarization for the WEAK input (which cannot depolarize on its own)

Front 27

What is the effect on LTP of blocking postsynaptic depolarization during a high frequency stimulation?

Back 27

Blocks LTP

LTP needs both presynaptic signal and postsynaptic depolarization

Front 28

What does the NMDA receptor require to open? (3)

When it opens, what flows through the NMDA receptor?

Back 28

1. Glutamate (NT)
2. Glycine (co-factor)
3. Depolarization (too move Mg from pore)

Allows Ca and Na through

Front 29

What happens with the NMDA and AMPA receptors in response to low frequency stimulation?

Back 29

Glutamate binds to AMPA --> open --> Na flows in

No current flows through the NMDA because of Mg blocking the pore

Front 30

What happens to AMPA and NMDA receptors during high frequency stimulation?

Back 30

Glutamate released, binds to AMPA
--> Na in --> depolarizes neuron --> pushes Mg out of NMDA receptor --> NMDA allows Ca in

Front 31

What is APV and what does it do to LTP induction?

Back 31

APV = NMDA receptor antagonist

Ca cannot enter, so LTP induction blocked

Front 32

What is BAPTA and what does it do to LTP induction?

Back 32

Ca chelator

Blocks LTP induction

Front 33

What are the 5 requirements for LTP induction under normal conditions?

Back 33

1. Presynaptic activation and glutamate release
2 .Significant postsynaptic depolarization
3. NMDA-receptor activation
4. Increase in Ca postsynaptically
5. Activation of Ca-regulated protein kinases (Ca-activated phosphorylation of AMPA receptor --> increase conductance)

Front 34

What are the 2 phases of LTP?

Back 34

1. First 2-3 hors driven by protein kinase activation by Ca

2. Longer lasting LTP requires transcription of new mRNA and synthesis of new proteins

Front 35

What do protein kinases do in early LTP?

Back 35

Phosphorylate AMPA glutamate receptors --> increased activity and increased numbers of AMPA receptors

Front 36

What is LTD and what causes it?

Back 36

LTD = long term depression

Caused by prolonged, low frequency stimulation --> NMDA receptor lets in small amount of Ca

Front 37

How are LTD and LTPs different in terms of dependence on Ca through the NMDA?

Back 37

High Ca through NMDA (high frequency stimulus) --> LTP

Low Ca through NMDA (low frequency stimulus) --> LTD

Front 38

What happens (with respect to LTD/LTP) with a medium stimulus?

Back 38

Neither LTP nor LTD; no change

Front 39

What is the mechanism by which LTP is induced by Ca?

Back 39

High Ca --> activates protein kinases --> phosphorylation of AMPA glutamate receptors --> increase activity and numbers --> LTP

Front 40

What is the mechanism by which Ca induces LTD?

Back 40

Low Ca --> protein phosphatase activation --> net decrease in phosphorylation of specific substrates