NEUR 0010 - Chapter 25

Question 1

What is nonassociative learning?

Answer 1

The change in behavioral response over time to a single type of stimulus

Question 2

What are the two types of nonassociative learning?

Answer 2

Habituation and sensitization

Question 3

What is associative learning?

Answer 3

When you form associations between two events

Question 4

What are the two types of associative learning?

Answer 4

Classical and operant conditioning

Question 5

What is classical conditioning?

Answer 5

Associating a stimulus that evokes a measurable response with a second stimulus that normally doesn’t evoke that response; using a US paired with a CS to evoke a CR

Question 6

What is instrumental conditioning? (Operant)

Answer 6

Associating a response (motor act) with a meaningful stimulus (reward)

Question 7

Based on the sea slug gill withdrawal reflex, where does habituation occur?

Answer 7

In the synapse between the sensory neuron and the motor neurons

Question 8

What did Kandel discover about the nature of habituation in the sensorimotor synapse?

Answer 8

That it’s caused by fewer quanta of synaptic vesicles released per AP, and thus is a presynaptic modificationi

Question 9

Based on the sea slug gill withdrawal reflex, how does sensitization occur?

Answer 9

Shock to the head synapses onto the sensory neuron’s axon terminal; releases serotonin to make more Ca2+ enter the sensory axon terminal by using cAMP/PKA to close K+ channels and allow more Ca2+ to have prolonged entry: causes more quanta of NT to be released

Question 10

What property of adenylyl cyclase makes it a good detector of CS-US coincidence?

Answer 10

It makes more cAMP in the presence of elevated Ca2+ concentration

Question 11

How does adenylyl cyclase contribute to associative learning?

Answer 11

Sensory axon terminal: allows in Ca2+ after the AP from the CS, influx of 5HT from the shocked neuron activates adenylyl cyclase from the US; since adenylyl cyclase increases with Ca2+, more cAMP and PKA are produced when the US is paired with the CS: causes more K+ channels to close, prolonged Ca2+ elevation, prolonged EPSP, and more quanta of NT released

Question 12

According to the sea slug associative learning hypothesis, what is learning vs memory?

Answer 12

Learning is when the CS causes elevated Ca2+ in coincidence with activated adenylyl cyclase from the US; Memory is when the K+ channels and closed and the NT release is enhanced

Question 13

What are the two layers of the cerebellar cortex?

Answer 13

Purkinje cell layer; granule cell layer

Question 14

What are Purkinje cells?

Answer 14

In the cerebellar cortex: dendrites only extend to the molecular layer; synapse on neurons in deep cerebellar nuclei (major output of cerebellum); use GABA as NT (inhibitory)

Question 15

What are the two sources of input to the cerebellar cortex?

Answer 15

Climbing fibers (from the inferior olive in the medulla) and Mossy fibers (from the pontine nuclei in the cerebral neocortex)

Question 16

What are climbing fibers?

Answer 16

From inferior olive to Purkinje cells: makes hundreds of large EPSPs that always activate Purkinje cell;

Question 17

What are mossy fibers?

Answer 17

From pontine nuclei to cerebellar granule cells: relay info from the cerebral neocortex

Question 18

What are cerebellar granule cells?

Answer 18

Small, packed, numerous: give rise to parallel fiber axons that run along the Purkinje cell dendrite plane in the top layer of cerebellar cortex

Question 19

How many inferior olive climbing fibers contact each Purkinje fiber?

Answer 19

One climbing per Purkinje

Question 20

How many cerebellar granule parallel fibers contact each Purkinje fiber?

Answer 20

Many, but each parallel fiber touches the same Purkinje only once and briefly

Question 21

What is the Marr-Albus theory of motor learning?

Answer 21

Predicts plasticity of parallel fiber synapse if it is active at the same time as the climbing fiber input to the postsynaptic Purkinje cell

Question 22

What is long term depression in the parallel fiber synapses?

Answer 22

When pairing stimulation of the parallel fibers and climbing fibers, activation of the parallel fibers alone will cause a smaller postsynaptic response in the Purkinje cell; occurs ONLY in parallel fiber synapses that are active at the same time as climbing fibers (input specificity)

Question 23

What are the two major differences in sea slug associative learning and cerebellar LTD?

Answer 23

Slug = change occurs at presynaptic terminal, increases response; Cerebellum: change occurs at Purkinje dendrite, decreases response

Question 24

Where is the parallel fiber-Purkinje synapse modified? How?

Answer 24

Postsynaptic: on the Purkinje dendrite; decreased postsyn response to glutamate from the parallel fibers; glutamate receptor that mediated EPSP si AMPA: internalized by the postsyn cell following LTD induction, so the synapse is less sensitive to glutamate

Question 25

What kind of glutamate receptor is responsible for the LTD in parallel fiber-Purkinje synapses?

Answer 25

AMPA receptors: internalized following LTD induction, making the Purkinje less sensitive to glutamate and decreasing the response

Question 26

What happens, molecularly, when the climbing fiber sends an AP to the Purkinje cell?

Answer 26

Very strong EPSP: opens up the Na+ channels to conduct an AP, BUT ALSO opens Ca2+ channels

Question 27

What happens, molecularly, when the parallel fiber synapses on the Purkinje cell?

Answer 27

Parallel fiber releases glutamate, to reach the AMPA receptors on the Purkinje cell membrane (these allow Na+ in after the climbing fiber conducts an EPSP), but another glutamate receptor (metabotropic) couples with G-protein and PLC to create PKC

Question 28

What three molecular events converge to cause LTD?

Answer 28

Increased Purkinje dendrite [Ca2+] from the climbing fiber; Increased [Na+] due to AMPA receptor activation from glutamate release by the parallel fiber; Increased PKC created by the G-protein/PLC cascade from the metabotropic glutamate receptors on the Purkinje dendrite membrane

Question 29

What do increased [Na+], increased [Ca2+], and increased PLC do to cause LTD in cerebellar cortex?

Answer 29

Cause a decrease in AMPA receptors: make the Purkinje cell dendrite less receptive to glutamate

Question 30

What are the two sheets of the hippocampus?

Answer 30

Dentate gyrus and Ammon's horn

Question 31

What is the dentate gyrus?

Answer 31

One of the sheets of the hippocampus

Question 32

What is Ammon's horn?

Answer 32

One of the sheets of the hippocampus; has four divisions, CA1-4

Question 33

What is one of the major inputs to the hippocampus?

Answer 33

Entorhinal cortex

Question 34

By what path does the entorhinal cortex input to the hippocampus?

Answer 34

The perforant path

Question 35

What is the perforant path?

Answer 35

Input from the entorhinal cortex to the hippocampus: its axons synapse on the neurons of the dentate gyrus, which sends mossy fiber axons to CA3 in Ammon's horn, which branch and send axons to the fornix and CA1 (Schaffer collateral)

Question 36

Describe the steps of the perforant path.

Answer 36

Entorhinal cortex sends axons to the dentate gyrus, which send mossy fiber axons to CA3 in Ammon's horn, which sends axons to the fornix and sends the Schaffer collateral axons to CA1

Question 37

What are the properties of LTP in CA1?

Answer 37

Caused by tetanus (rapid frequency APs) to presynaptic Schaffer collateral axons; causes a greater EPSP than expected; lasts for weeks to a lifetime; doesn't require high-frequency APs (but does require that the synapse is active at the same time as the postsynaptic CA1 neuron is strongly depolarized)

Question 38

What two conditions are necessary for an LTP to occur in a Schaffer collateral presynaptic axon - CA1 synapse?

Answer 38

1) synapses must be stimulated at frequency high enough to cause temporal summation of EPSPs, and 2) enough synapses must be stimulated together to cause spatial summation (cooperativity)

Question 39

What two things must occur simultaneously for an LTP to occur between Schaffer collateral axon and CA1?

Answer 39

Synapse must be active at the SAME time that the postsynaptic CA1 neuron is strongly depolarized

Question 40

What neuroscience saying is indicative of the creation of LTPs between Schaffer collateral axons and CA1?

Answer 40

Fire together, wire together!

Question 41

How does EPSP transmission differ in the CA1 pyramidal cells from the cerebellar cortex cells?

Answer 41

In addition to containing AMPA receptors, also contain NMDA receptors

Question 42

Why is it significant that CA1 pyramidal cells contain both AMPA and NMDA glutamate receptors?

Answer 42

NMDA receptors conduct Ca2+ IFF glutamate binds and the postsynaptic membrane is depolarized enough to displace the magnesium block: WHICH MEANS: only allows Ca2+ through when the presynaptic and postsynaptic elements are active simultaneously

Question 43

What does the rise in [Ca2+] in the postsynaptic element during EPSP transduction using NMDA receptors create?

Answer 43

PKC and CaMKII (calmodulin dependent protein kinase II)

Question 44

What is the BCM theory?

Answer 44

Accounts for the bidirectional regulation of synaptic strength; synapses that are active when the postsynaptic cell is weakly depolarized undergoes LTD instead of LTP

Question 45

How does [Ca2+] influx cause both LTP and LTD?

Answer 45

Level of NMDA activation and Ca2+ influx: if the cell is weakly depolarized, the Mg2+ block isn't moved from the NMDA receptors, so only a little Ca2+ in (causes LTD); if cell highly depolarized, Mg2+ block completed moved, and Ca2+ floods in (causes LTP)

Question 46

What opposing actions for Ca2+ cause to create LTD vs LTP?

Answer 46

Low Ca2+ activates protein phosphatases to cause dephosphorylation (LTD), whereas high Ca2+ activates PKC and CaMKII to phosphorylate (LTP)

Question 47

What is the molecular switch hypothesis?

Answer 47

The idea that an autophosphorylating kinase can store info at the synapse by keeping its "pocket knife" configuration open

Question 48

When is new protein synthesis most critical for LTM formation?

Answer 48

During the consolidation period after training

Question 49

What is CREB?

Answer 49

A protein transcription factor: cAMP response element binding protein

Question 50

What does CREB do?

Answer 50

Binds to specific DNA segments (cyclic AMP response elements, or CREs) and regulates the expression of neighboring genes

Question 51

What are the two different forms of CREB, and what does each do?

Answer 51

CREB-2 (represses gene expression when bound to the CRE) and CRED-1 (activates transcription IFF phosphorylated by PKA)