Synaptic Transmission In The Cns

Front 1

Where are the cell bodies of the neurons of the NMJ?

Back 1

They are typically located in the ventral horn of the spinal cord.

Front 2

T/F:
Each muscle fiber is innervated by a single neuron, and each motoneuron contacts only a single muscle fiber.

Back 2

False: Each muscle fiber is contacted by a single motoneuron, but each motoneuron may innervate many muscle fibers.

Front 3

T/F:
An EPP is always large enough to generate an AP on the muscle fiber.

Back 3

True

Front 4

Is the activity of a single synpase sufficient to generate a post-synaptic AP in the CNS?

Back 4

No - the interactions of several synapses are required to generate a post-synaptic AP in the CNS.

Front 5

T/F:
Synapses in the CNS and at the NMJ can generate inhibitory as well as excitatory signals.

Back 5

False: CNS synapses may be inhibitory or excitatory, but those at the NMJ are excitatory only.

Front 6

How does an IPSP work?

Back 6

It causes K+ and Cl- channels to open, which hyperpolarizes the post-synaptic neuron, thus increasinng the stimulation required to reach threshold.

Front 7

Describe temporal summation. Where does this occur - the CNS or NMJ?

Back 7

*Repeated activation of the same synapse results in addition of signals
*occurs in the CNS

Front 8

Describe spatial summation. Where does it occur - the CNS or NMJ?

Back 8

The post-synaptic neuron receives signals from multiple synapses which add algebraically
*occurs in the CNS

Front 9

Name three amino acid neurotransmitters used in the CNS. Are they generally excitatory or inhibitory?

Back 9

1. Glycine - inhibitory
2. Glutamate - excitatory
3. GABA - inhibitory

Front 10

Though specific neurotransmitters are generally excitatory or inhibitory, what ultimately determines their effect?

Back 10

The nature of the receptor on the post-synaptic neuron.

Front 11

Name three neuropeptides commonly used as neurotransmitters in the CNS.

Back 11

*somatostatin
*substance P
*CGRP

Front 12

Name three monoamines commonly used as neurotransmitters in the CNS.

Back 12

*epinephrine
*norepinephrine
*serotonin
(*dopamine)

Front 13

What are two gases that operate as neurotransmitters in the CNS?

Back 13

*nitric oxide
*carbon monoxide

Front 14

Describe the structure of an ionotropic receptor. How long does stimulation of receptors of this class last?

Back 14

*the neurotransmitter receptor is itself an ion channel that opens or closes when bound
*thus, the receptor is a ligand-gated ion channel
*effects are short (millisec)

Front 15

Name three neurotransmitters whose receptors are usually ionotropic.

Back 15

*ACh
*glycine
*serotonin
*GABA

Front 16

Describe the structure of a metabotropic neurotransmitter receptor. Does stimulation have long or short effects?

Back 16

*the receptor is a separate molecule from the affected ion channel
*the two may be connected by G-protein interaction
*usually generates long-lasting effects (minutes to hours)

Front 17

What are three neurotransmitters whose receptors are usually metabotropic?

Back 17

*norepinephrine
*epinephrine
*dopamine
*neuropeptides

Front 18

Name the two main classes of glutamate receptor. Which is excitatory and which is inhibitory? Will a single synapse have only one or both classes?

Back 18

*NMDA and AMPA
*both are excitatory
*a given synapse usually contains both classes in varying proportions

Front 19

Describe the activity of the AMPA receptor. What is the duration of its effects?

Back 19

*it is an ionotropic receptor that allows passage of K+ and Na+ when stimulated, causing a post-synaptic depolarization
*effects are short: 10-20 milliseconds

Front 20

Name the two co-agonists involved in transmission across a NMDA receptor. How are the concentrations of these molecules thought to be controlled?

Back 20

*glycine and d-serine
*thought to be regulated by neuroglia

Front 21

What blocks the channel of the NMDA receptor when it is at RMP? How is this block removed?

Back 21

*the channel is blocked by a Mg++ ion
*depolarization of the membrane by stimulation of AMPA or some other way causes the Mg++ to leave

Front 22

On the molecular level, what happens when a NMDA receptor is stimulated?

Back 22

*its channel opens and allows entry of Na+ and Ca++
*Ca++ is able to modulate a number of intracellular pathways

Front 23

What is LTP? What is the critical event leading to it?

Back 23

*long-term potentiation: long-lasting changes in the excitability of the post-synaptic neuron
*removal of the Mg++ ion and entry of Ca++ is key

Front 24

Can LTP occur even in the absence of glutaminergic stimulation?

Back 24

Yes - if the post-synaptic neuron is sufficiently depolarized to remove the Mg++ ion from the NMDA channel and allow entry of Ca++.

Front 25

How might LTP be induced by temporal summation? By spatial summation?

Back 25

*in temporal summation, tetanization of pathways may potentiate the response
*in spatial summation, the response may be potentiated by the association of several pathways

Front 26

What are two ways that LTP may be the result of post-synaptic effects?

Back 26

*addition of new AMPA receptors or activation of old receptors on the post-synaptic neuron
*interaction of metabotropic NMDA receptors with ionotropic ones
*modification of AMPA receptors to increase Ca++ conductance
*all of these result in more ion flow for a given amount of glutamate in the cleft

Front 27

What is one of the drawbacks of LTP?

Back 27

It may prevent a synapse from participating in other experience-dependent activities.

Front 28

What reduces LTP? How does this occur?

Back 28

*long term depression (LTD)
*stimulation of a glutaminergic synapse at very low frequencies (~1 Hz) which causes a decline in response amplitude

Front 29

How is glutamate neurotoxic in high extracellular concentrations?

Back 29

It causes a dramatic increase in the entry of Ca++ into the neuron which then induces apoptotic pathways.

Front 30

What are two events that can cause a dangerous rise in the extracellular concentration of glutamate?

Back 30

Trauma or CVA causing cell damage and release of glutamate into the extracellular space.

Front 31

Where is the point of lowest threshold on a CNS neuron?

Back 31

At the axon hillock

Front 32

What are two ways the excitability of a CNS neuron may be biased?

Back 32

1. Change the tonic level of excitation or inhibition
2. Use drugs to change bias

Front 33

How is LTP thought to modulate long-term learning?

Back 33

Protein re-folding is thought to occur at synapses undergoing LTP. This effects a more permanent change in the pathway.