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