These questions are NOT for homework; they are simply for you to use as a study tool.
Be sure you can answer all questions completely.
1. What is the proposed membrane topology for voltage-gated sodium channels? And what is it for Shaker potassium channels?
2. What evidence is there that voltage-gated sodium, potassium, and calcium channels are related?
3. What part of the sodium channel forms the pore? What part of the potassium channel forms the pore? How would you prove it?
4. What accounts for ionic selectivity? What are their molecular bases? What is the key difference between potassium channels and sodium channels?
5. Can you alter the ion selectivity of an ion channel? Explain.
6. What part of the voltage-gated channel forms the voltage sensor? Why do you think so?
7. What could you do experimentally (or what has already been done) to prove that this part of the channel is the one actually responsible for sensing voltage?
8. How is the channel activated by voltage changes?
9. Are all ion channels voltage-sensitive? If not, why aren't they?
10. How do sodium and potassium channels inactivate? Could you identify the molecular basis of channel inactivation?
11. What is voltage clamp? What could you learn about an action potential from voltage-clamp analysis? (assume that you vary the voltage from –70 mV to +70 mV, with 10 mV/step and that the neuron only has a fast sodium current and a delayed rectifier potassium current).
12. If you treat a squid giant axon with TTX, what kind of current-voltage (I-V) plot do you get? Why?
13. If you treat a squid giant axon with TEA, what kind of current-voltage (I-V) plot do you get? Why?
14.What is reversal potential? What is Erev for sodium? What is Erev for potassium? Could you
use them to explain the amplitude of an action potential?
15. What will happen to the action potential shape if you partially reduce the amount of potassium currents?
16. Draw an action potential. Label the following on your diagram: sodium channel activation, sodium channel inactivation, sodium channel closure, potassium channel activation, potassium channel closure.
17. What are gating currents? Are they carried by charged ions such as sodium and potassium? Do they have a threshold for activation?
18. Draw five traces of single channel currents from a voltage-gated sodium channel activated at +20 mV (from VH = -70 mV)? Compare them with the macroscopic current you obtained from voltage-clamp at the same depolarizing voltage. How do they differ?
19. Could you use molecular terms to explain the refractory period of action potentials?
Study Questions for `Other Ion Channels and Intrinsic Membrane Properties of Neurons' and `Ion Channels and Disease'
1. What are considered the major factors that determine the personality (i.e. intrinsic membrane properties) of neurons?
2. What are the minimal requirements of ion channel types for a tonically active neuron?
3. What are the minimal requirements of ion channel types for a rhythmically bursting neuron?
4. What is so special of low-voltage activated ion channels? Could you give a few examples of this kind of ion channels?
5. Are channels always activated by depolarizations? If not, could you give two examples?
6. What is so special of the transient potassium current (IA)? Could you explain it using your molecular biology knowledge?
7. Give one unique feature of Ca2+-activated potassium current.
8. What is afterhyperpolarization (AHP)? What are the cause and usefulness of it?
9. Is inward rectifying potassium current identical to Ih? What are their differences?
10. What is dendrite? Is it passive? How would a neuron use it to tune its own activity?
11. How would one obtain the activation and inactivation curves of an ion channel experimentally? Use voltage-gated sodium channel as an example.
12. What is reversal potential? How would one determine the reversal potential for voltage-gated sodium currents?
13. Draw a current-voltage plot for each type of K channel (delayed rectifier, transient potassium channel, inward rectifier, and Ca2+-activated potassium channel).
14. What does it mean that one of the sodium currents is transient and that one is persistent?
15. What important consequence does the refractory period have for the conduction of action potentials?
16. How does changing Ih affect neuronal firing?
17. How does changing the delayed rectifier affect neuronal firing?
18. How would you change the frequency of neuronal firing?
19. What are specific examples of how modifications of channel properties lead to pathologies? Use sodium channel as an example.
20. How might mutations in general affect channel properties (for example, a mutation in the promoter region might cause the over or under expression of a certain ion channel)?
Study Question for Mechanisms of Synaptic Transmission
1. Discuss the structure and function of electrical synapses.
2. What advantages might electrical synapses have over chemical synapses?
3. What steps are involved in chemical synaptic transmission?
4. What currents might be responsible for excitatory synapses? What currents might be responsible for inhibitory synapses?
5. In what ways are inputs integrated? What is the purpose of integrating inputs?
6. What do you usually find in the presynaptic terminal? What is an active zone?
7. Describe the interaction of sodium and potassium at the neuromuscular junction. Include the following terms in your description: ACh, reversal potential, EPSP.
8. Describe the evidence supporting vesicle fusion with the presynaptic membrane.
9. If calcium blockers are applied to the axon, what effect will this have on synaptic transmission if the axon undergoes an action potential?
10. What are the differences between an EPSP and an IPSP? What determines whether a specific transmitter is excitatory or inhibitory?
11. What is shunting? Explain it using the Ohms law.
12. What are the two essential components of the vesicle hypothesis?
13. What do you expect to see on the presynaptic terminal membrane using freeze-fracture techniques when a) the nerve is not stimulated and b) the nerve is intensely stimulated?
14. What is capacitance? What would an increase in membrane capacitance suggest?
15. What is a quantum? What is quantal release?
16. What is a MEPP? How does this differ from an EPSP?
17. What is the evidence that calcium is required for vesicle exocytosis?
18. What is the core complex? What are its components?
19. What is SNARE? How many SNARE proteins do you find in nerve terminals? Which one is v-SNARE and which is (are) t-SNAREs?
20. Why do dermatologists use botulinum toxins to reduce wrinkles and keep their patients `youthful'? What do these toxins do to SNARE proteins?
21. What is the SNARE hypothesis? Why do we think it is no longer correct?
22. What evidence do we have to suggest that SNARE proteins are important for vesicle fusion?
23. What are the advantages and disadvantages of `knock-out' experiments?
24. What is synaptotagmin? Why is it suggested to be a calcium sensor?
25. Is synaptotagmin the only calcium sensor? If not, why?
26. Why do you need to recycle synaptic vesicles in nerve terminals?
27. What is clathrin? How does it endocytose synaptic vesicles?
28. How might the homogeneous sized vesicles be regulated?
29. What is dynamin? What roles does it play during vesicle recycling?
30. What impacts would defects in endocytosis and recycling have on vesicle exocytosis?