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Synaptic Transmission in the CNS


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Where are the cell bodies of the neurons of the NMJ?
They are typically located in the ventral horn of the spinal cord.
Each muscle fiber is innervated by a single neuron, and each motoneuron contacts only a single muscle fiber.
False: Each muscle fiber is contacted by a single motoneuron, but each motoneuron may innervate many muscle fibers.
An EPP is always large enough to generate an AP on the muscle fiber.
Is the activity of a single synpase sufficient to generate a post-synaptic AP in the CNS?
No - the interactions of several synapses are required to generate a post-synaptic AP in the CNS.
Synapses in the CNS and at the NMJ can generate inhibitory as well as excitatory signals.
False: CNS synapses may be inhibitory or excitatory, but those at the NMJ are excitatory only.
How does an IPSP work?
It causes K+ and Cl- channels to open, which hyperpolarizes the post-synaptic neuron, thus increasinng the stimulation required to reach threshold.
Describe temporal summation. Where does this occur - the CNS or NMJ?
*Repeated activation of the same synapse results in addition of signals
*occurs in the CNS
Describe spatial summation. Where does it occur - the CNS or NMJ?
The post-synaptic neuron receives signals from multiple synapses which add algebraically
*occurs in the CNS
Name three amino acid neurotransmitters used in the CNS. Are they generally excitatory or inhibitory?
1. Glycine - inhibitory
2. Glutamate - excitatory
3. GABA - inhibitory
Though specific neurotransmitters are generally excitatory or inhibitory, what ultimately determines their effect?
The nature of the receptor on the post-synaptic neuron.
Name three neuropeptides commonly used as neurotransmitters in the CNS.
*substance P
Name three monoamines commonly used as neurotransmitters in the CNS.
What are two gases that operate as neurotransmitters in the CNS?
*nitric oxide
*carbon monoxide
Describe the structure of an ionotropic receptor. How long does stimulation of receptors of this class last?
*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)
Name three neurotransmitters whose receptors are usually ionotropic.
Describe the structure of a metabotropic neurotransmitter receptor. Does stimulation have long or short effects?
*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)
What are three neurotransmitters whose receptors are usually metabotropic?
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?
*both are excitatory
*a given synapse usually contains both classes in varying proportions
Describe the activity of the AMPA receptor. What is the duration of its effects?
*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
Name the two co-agonists involved in transmission across a NMDA receptor. How are the concentrations of these molecules thought to be controlled?
*glycine and d-serine
*thought to be regulated by neuroglia
What blocks the channel of the NMDA receptor when it is at RMP? How is this block removed?
*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
On the molecular level, what happens when a NMDA receptor is stimulated?
*its channel opens and allows entry of Na+ and Ca++
*Ca++ is able to modulate a number of intracellular pathways
What is LTP? What is the critical event leading to it?
*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
Can LTP occur even in the absence of glutaminergic stimulation?
Yes - if the post-synaptic neuron is sufficiently depolarized to remove the Mg++ ion from the NMDA channel and allow entry of Ca++.
How might LTP be induced by temporal summation? By spatial summation?
*in temporal summation, tetanization of pathways may potentiate the response
*in spatial summation, the response may be potentiated by the association of several pathways
What are two ways that LTP may be the result of post-synaptic effects?
*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
What is one of the drawbacks of LTP?
It may prevent a synapse from participating in other experience-dependent activities.
What reduces LTP? How does this occur?
*long term depression (LTD)
*stimulation of a glutaminergic synapse at very low frequencies (~1 Hz) which causes a decline in response amplitude
How is glutamate neurotoxic in high extracellular concentrations?
It causes a dramatic increase in the entry of Ca++ into the neuron which then induces apoptotic pathways.
What are two events that can cause a dangerous rise in the extracellular concentration of glutamate?
Trauma or CVA causing cell damage and release of glutamate into the extracellular space.
Where is the point of lowest threshold on a CNS neuron?
At the axon hillock
What are two ways the excitability of a CNS neuron may be biased?
1. Change the tonic level of excitation or inhibition
2. Use drugs to change bias
How is LTP thought to modulate long-term learning?
Protein re-folding is thought to occur at synapses undergoing LTP. This effects a more permanent change in the pathway.

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