Problem Set 2 - Action Potential, MEPP


Physiology Facilitator Problem Set 2

Action potential, motor endplate potential, transport

 

 

The first eight questions ask information regarding the figure below. To keep things simple, assume that currents produced by only two ions, K+ and Na+, contribute to this squid action potential.

 

 

1. The straight dashed line at about –80 mV represents the equilibrium potential for what ion?.

 

2. The straight dashed at about + 65 mV represents the equilibrium potential for what ion?

 

3. What does curve T represent?

 

4. What does curve U represent?

 

5. What prevents the “peak” of the action potential from reaching ENa?

 

6. What causes EM to be more negative at point W than it was prior to the initiation of the action potential?

 

7. What is the reason that a normally suprathreshold stimulus if given at a time corresponding to the upward arrow on the X axis will not elicit another action potential?

 

8. In terms of the abbreviated Chord equation given below, describe the events that change EM during the entire action potential.

 

Chord equation: EM = ENa (gENa/gEtotal) + EK (gEK/gEtotal)

 

9. An action potential will propagate from its site of initiation in the cell body of a spinal cord motorneuron to the presynaptic terminal at the neuromuscular endplate (i.e. anterograde propagation), but upon depolarizing the presynaptic terminal, the action potential does not repropagate back to the cell body (i.e., retrograde propagation) Why is this?

 

 

For the next several questions you may wish to refer to the figure below.

 

 

10. As a motoneuron-action potential reaches the end of the axon:

 

11. In view of the fact that acetylcholine opens non-selective cation-channels in the postsynaptic membranes, what causes the postsynaptic membrane to depolarize, i.e., shouldn't inward Na+ current match outward K+ current?

 

12. Define miniature end-plate potential (MEPP). Define end-plate potential (EPP). What can modify the frequency of MEPPs? What can modify the amplitude of EPPs?

 

13. Where in the synapse is acetylcholine-esterase located? How would administering an effective acetylcholinesterase inhibitor alter the amplitude and frequency of the MEPPs? How would the magnitude of the EPP be altered?

 

 

 

 

 

 

Select the SINGLE BEST answer.

 

In answering the following next three questions, assume that if a presynaptic vesicle is released and its acetylcholine reaches and opens some channels in the motor end plate, a MEPP will result, and no matter how small the resulting MEPP, it is still considered to be a MEPP.

 

14. Curare binds to and blocks the acetylcholine receptor at the neuromuscular junction. An isolated nerve muscle preparation treated with a less-than-saturating dose of curare would be associated with a decrease in the:

 

15. An isolated nerve-muscle preparation exposed to a low concentration of extracellular Ca2+ would be associated with a decrease in the:

 

16. The endplate potential (EPP) that normally occurs at a vertebrate neuromuscular junction:

 

17. The unequal distribution of Na+ and K+ across a resting, excitable membrane:

 

18. A counter transport mechanism that exchanges one extracellular Na+ for one intracellular H+ in the membrane of a cell whose resting potential is -60 mV and whose intracellular [Na+] is 12 mM and extracellular [Na+] is 120 mM can achieve what maximum theoretical pH gradient across the cell membrane? (Remember that pH = -log [H+], for example, pH = 7 means [H+] = 10-7M.)

 

19. A sodium-coupled amino acid cotransport mechanism exists that transports one Na+ ion inward for each glycine molecule that is transported inward. Since one positive charge is transported inward for each cycle of the cotransport mechanism, what theoretical maximum internal concentration of glycine could be achieved when there is an external glycine concentration of 1 mM and the cell has a resting potential of -60 mV, an internal [Na+] of 12 mM and external [Na+] of 120 mM?