《神经学》英文课后作业 3 Synaptic Transmission.docx

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1、Homework3-20161. Are synaptic vesicles delivered to the nerve terminal by slow or fast axonal transport? Explain. Fast.Neuorpeptide precursors and enzymes are synthesized in the cell body of neuron, and then transported in vesicles down a long way to the axon terminal, which requires a fast axonal t

2、ransport.2. List the steps involved in chemical neurotransmission.Transmitter is synthesized and then stored in vesiclesAn action potential invades the presynaptic terminalDepolarization of presynaptic terminal causes opening of voltage-gated Ca2+ channelsInflux of Ca2+ through channelsCa2+ causes v

3、esicles to fuse with presynaptic membraneTransmitter is released into synaptic cleft via exocytosisTransmitter binds to receptor molecules in postsynaptic membraneOpening or closing of postsynaptic channelsPostsynaptic current causes excitatory or inhibitory postsynaptic potentialRetrieval of vesicu

4、lar membrane from plasma membrane3. What is the significance of the quanta! nature of MEPPs? What is the evidence that EPPs are composed of MEPPs?(a) It helped find out that the neurotransmitter that causes EPPs is released from vesicles.(b) When axon is stimulated, postsynaptic membrane potentials

5、(EPPs) responding to the stimulation is recorded as times of the spontaneous potentials (MEPPs).4. What Unes of evidence suggest that neurotransmitters are released from synaptic vesicles?When stimulation was treated, vesicles fusing with plasma membrane were found increased through the microscope,

6、and the number of this fusing was proportional to the number of quantal release of neurotransmitters.5. Summarize the experimental evidence that synaptic vesicles are recycled in the axon terminal. With the addition of horseradish peroxidase (HRP) in extracellular solution to indicate color change a

7、nd a brief stimulation of presynaptic terminal, HRP was found fused into the axon terminal in vesicles and circulated from cytosol to endosome, then back to cytosol again, and finally released.6. It has been demonstrated that a rise in presynaptic Ca2+ is necessary and sufficient for neurotransmitte

8、r release. What experimental evidence supports the claim that Ca2+ is necessary? Sufficient?(a) When injected Ca2+ channel blocker (cadmium) or Ca2+ chelator (BAPTA) into the presynaptic terminal, postsynaptic membrane potential was found almost vanished.(b) Injecting Ca2+ into presynaptic terminal

9、causes depolarization of the postsynaptic membrane,even in the absence of presynaptic action potential.7. Indicate how each of the following are involved in neurotransmitter secretion:SNAP-25: contributes two a-helices to the four of the SNARE complex, which helps prime synaptic vesicles to the memb

10、rane.Synaptobrevin vesicular SNARE, contributes one a-helices to the SNARE complex Synaptotagmin: serves as a calcium sensor and regulates intimately the SNARE zipping Synapsin . reversibly binds to synaptic vesicles, may cross-link newly formed vesicles to the cytoskeleton to keep the vesicles teth

11、ered within the reserve pool. Mobilization of these reserve pool vesicles is caused by phosphorylation of synapsin by proteins kinases, which allows synapsin to dissociate from the vesicles, thus freeing the vesicles to make their way to the plasma membrane. Which one is key in the regulation of tra

12、nsmitter release by C/?SynaptotagminKey Termsacetylcholine (ACh) botulinum toxin clathrinco-transmitterdynaminend plateend plate current (EPC)end plate potential (EPP)EPSPexcitatoryfast axonal transport gap junction inhibitoryionotropic receptorlarge dense-core vesicles ligand-gated ion channel mini

13、ature end plate potential (MEPP) neurotransmitterpostsynapticpostsynaptic current (PSC) postsynaptic potential (PSP) presynapticreceptor moleculereversal potential slow axonal transport small clear-core vesicle SNAP-25 synaptic cleft synaptic vesicle synaptic vesicle cycle synaptobrevin synaptotagmin tetanus toxin