Learning & Memory

Front 1

What is a mechanism for memory storage?

Back 1

Neural plasticity.

Front 2

What is neurogenesis?

Back 2

The birth of new neurons when you learn new information. Thought to encode new memories.

Front 3

What is the problem with the idea of neurogenesis?

Back 3

You would have to have a tiny brain with lots of empty space so you have room to build more and more neurons for learning. However, neurogenesis does occur in the brain until death.

Front 4

What brain region(s) shows lots of neurogenesis?

Back 4

Hippocampus and Olfactory bulb. But, neurons also die and some that are born do not survive throughout adult life span.

Front 5

What is synaptic plasticity?

Back 5

Changes in the structure and/or function of existing synapses or the new growth of new synapses.

Front 6

How do synapses associate with learning?

Back 6

Synaptic strength between neurons. Number of synapses. Change structure/function.

Front 7

How does the brain store information via synaptic plasticity?

Back 7

Changes in existing synapses - presynaptic release, postsynaptic sensitivity, synapse change.

Front 8

What is synaptogoenesis?

Back 8

Change sin the number of synapses - more contacts, rearrangement of contacts.

Front 9

What did Mark Rosenzweig study with plasticity in brain?

Back 9

Had animals housed in different conditions (impoverished, social, and enriched). The animals housed in the enriched environments had greater cortical thickness, dendritic branching, and number of synapses.

Front 10

What real life application does Mark Rosenzweig's work have?

Back 10

Head start programs - learning environments

Front 11

What are Hebbian synapses?

Back 11

Synapses that become strengthened because one cell repeatedly takes part in firing another cell.

Front 12

What is long-term potentiation?

Back 12

Increase in synaptic transmission induced by high-frequency electrical stimulation. (Higher EPSP)

Front 13

What is unique about long-term potentiation?

Back 13

The change in synaptic transmission lasted for hours. Occurs in structure important for memory (hippocampus)

Front 14

What is the cooperativity property of LTP?

Back 14

probability of inducing LTP is related to number of stimulated afferents. More afferents = better LTP

Front 15

What is input-specificity property of LTP?

Back 15

LTP is restricted to tetanized synapses. (Only those stimulated)

Front 16

What is the associativity property of LTP?

Back 16

Weak pathways support LTP if paired with strong pathways.

Front 17

What property of LTP can be associated with classical conditioning?

Back 17

Associativity property

Front 18

What does LTP require?

Back 18

Presynaptic activity + postsynaptic depolarization produces LTP

Front 19

What are NMDA receptors?

Back 19

Hebbain receptors that open when there is presynaptic glutamate and postsynaptic depolarization.

Front 20

Why are NMDA receptors Hebbian?

Back 20

They open when there is presynaptic glutamate and postsynaptic depolarization. Activity in both pre and post synaptic cells.

Front 21

The associative property of LTP is analogous to....?

Back 21

Classical conditioning. Weak pathway - CS; strong pathway - US

Front 22

What is the entorhinal cortex?

Back 22

multimodal cortex - has every sense represented in it. Main input into the hippocampus.

Front 23

What is the preferred area of the hippocampus to be studied?

Back 23

The CA1 schaffer collateral cells.

Front 24

Is the trisynaptic circuit in the hippocampus open or closed?

Back 24

It is a open circuit. Entorhinal - dentate gyrus - CA3 - CA1 - Entorhinal - so on

Front 25

What is tetanus?

Back 25

High-frequency presynaptic stimulation

Front 26

What mediates excitatory synaptic transmission?

Back 26

L-glutamate

Front 27

What are AMPA and kainate receptors?

Back 27

Ionotropic glutamate receptors that are ligand-gated and have a fast Na+ current.

Front 28

What are NMDA receptors?

Back 28

Ionotropic glutamate receptors that are voltage and ligand-gated. Mg++ blocks these receptors at hyperpolarized membrane potentials. They have a late onset and a slowly decaying current. Must have postsynaptic membrane depolarize for binding.

Front 29

Which receptor does the majority of the work for synaptic transmission?

Back 29

AMPA receptors because NMDA receptors are blocked by Mg++

Front 30

How do the NMDA receptors become unblocked?

Back 30

Intense activation of AMPA receptors strongly depolarizes postsynaptic cell.

Front 31

How is the LTP produced via NMDA receptors?

Back 31

Ca++ influx through the receptors

Front 32

What is an important kinase for LTP?

Back 32

Calcium-calmodulin dependent kinase II

Front 33

During which rhythm is optimal for LTP induction?

Back 33

Theta rhythm

Front 34

What is feed-forward inhibition?

Back 34

Shuts down depolarized neuron before it gets too out of control (mediated by inhibitory interneurons)

Front 35

What synaptic changes cause LTP?

Back 35

Increased presynaptic release of glutamate and/or increased postsynaptic sensitivity.

Front 36

What are two modes of induction of LTP?

Back 36

Electrical and Chemical

Front 37

How is electrical stimulation used for LTP?

Back 37

Using a high-frequency stimulation on the presynapse or pairing low-frequency presynaptic stimulation with a postsynaptic depolarization.

Front 38

What are the temporal components of LTP?

Back 38

Post-tetanic potentiation - short-lived synaptic plasticity. Short & Long lasting LTP

Front 39

Describe LTP Induction

Back 39

Transmission requires the binding of glutamate receptors to AMPA & NMDA receptors...a necessary but not sufficient requirement. NMDA is bloked by Mg++, but when AMPA is highly activated you get depolarization which unplugs the NMDA receptor from Mg++ and allows an influx of Ca++

Front 40

What is long-term depression?

Back 40

Extensive low-frequency stimulation weakens synaptic connection. Just like LTP, NMDA receptors must be working. If there is low calcium via phosphotase activation, LTD will occur.

Front 41

What two factors may cause LTP?

Back 41

More presynaptic release of glutamate and/or postsynaptic sensitivity with more AMPA receptors for binding after LTP

Front 42

Post-translational modifications

Back 42

Assembling or modifying existing parts

Front 43

Transcription & Translation

Back 43

Processes that make new parts

Front 44

What are the pathways to plasticity?

Back 44

Stimulation - synapse activity - biochemical interactions - assembling and generating via post-translational modifications and transcription/translation - enhanced AMPA receptor function - strengthened synapses - LTP

Front 45

What is AMPA trafficking?

Back 45

Some AMPA receptors are found in the cytoplasm where glutamate cannot bind to them. However, their location is not static as they can move in and out of the plasma membrane

Front 46

What are silent synapses?

Back 46

Synapses without AMPA receptors - thus no glutamate binding.

Front 47

What special role does Ca++ play?

Back 47

It can modify pre-existing proteins - post-translational modification

Front 48

What is calmodulin?

Back 48

a calcium-binding protein that can regulate a number of protein targets.

Front 49

What are kinases important for?

Back 49

Altering proteins via phosphorlyation - phosphorlyation changes shape of a protein, thus changing its functional properties

Front 50

What is CaMKII?

Back 50

One of the most important kinases involved in the induction of LTP - if it is inhibited LTP cannot occur.

Front 51

CaMKII can enhance synapse strength by modifying what?

Back 51

AMPA receptors - in several different ways.

Front 52

What is the importance of GluR1 AMPA subunit?

Back 52

Has a large contribution to synaptic potentials because when it is phosphorylated by CaMKII, the channel conductance is enhanced which makes it more likely to open when glutamate binds to it.

Front 53

How are GluR1 receptors trafficked into dendritic spines?

Back 53

PKA phsophorylation of the P3 site moves them into the extrasynaptic region. Then, the influx of Ca++ from NMDA receptors activates PKC, which phosphorylates the P1 area which anchors them into the PSDZ.

Front 54

What two processes are required for Long-lasting LTP?

Back 54

Transcription (converting genetic material from DNA to mRNA) and translation (conversion of mRNA to proteins)

Front 55

What is genomic signaling?

Back 55

A high-frequency stimulation produces synaptic activity which activates signaling molecules. These molecules phosphorylate CREB protein. Transcription and translation occur and new proteins are produced that are essential for enduring changes.

Front 56

What happens when there is no CREB gene?

Back 56

L-LTP cannot be induced but S-LTP can. General conclusion - CREB protein transcribes mRNAs that are critical for long-lasting synaptic changes (PPs - plasticity products)

Front 57

Local protein synthesis

Back 57

Synaptic activity initiates protein synthesis (translation) immediately. Does not support genomic signaling theory. Translation of mRNAs that are already present -- translation of new protein takes place locally in the dendrites.

Front 58

What are the processes of combining genomic signaling and local protein synthesis ideas?

Back 58

High frequency stimulation generates synaptic activity which produces parallel effects of local translation of proteins already in the dendrite and a genomic cascade. The cascade generates phosphorylation of CREB protein which leads to transcription followed by translation (plasticity products)

Front 59

Synaptic tagging

Back 59

Biological processes tag the spines that were stimulated which tells the PPs where to go. However, strong stimulation is required to both tag and produce genomic signaling which produce the PPs.

Front 60

What must happen with tags and PPs to produce L-LTP?

Back 60

They must overlap.

Front 61

A Weak stimulus and its effects with synaptic tagging

Back 61

Generates S-LTP

Front 62

Weak stimulus given before or after Strong stimulus - synaptic tagging

Back 62

Produce L-LTP