Case Study #2 - The Neuron and Action Potentials Part I : Resting Membrane Poten

Question

Case Study #2 - The Neuron and Action Potentials

Part I: Resting Membrane Potential (3 pts ea)

For a normal, unstimulated neuron, there will be a larger concentration of __(1)___ ions outside of the neuron cell membrane and a larger concentration of __(2)_ ions just inside the neuron cell membrane. The resting membrane potential of a typical multipolar neuron is __(3)_ mV. The rmp is also due to the presence of active transport mechanisms on the neuron membrane called __(4)__. This transporter that is like a revolving door moves three __(5)__ ions outward and two __(6)___ ions inward. Finally, the intracellular location of negatively charged __(7)__ (macromolecules) determines the final rmp.

Part II: The Action Potential (3 pts ea)

The action potential begins with the neuron at resting membrane potential. If a stimulus occurs, the gates specific for the type of stimulus will start to open and allow ___(8)__ ions to enter. This causes the rmp to become less __(9)__ (charge) as it nears threshold. At threshold, __(10)__ voltage activated channels begin to open. In an example of __(11)___ feedback, more and more of these types of voltage activated gates will continue to open. Eventually, a voltage will be reached (+30 mV) at which these gates have closed. This phase of an action potential is called __(12)__.

At this time, __(13)___ voltage activated channels will open causing the peak of the action potential to turn downward. These channels continue to open until the voltage continues to decrease past threshold. This phase of the action potential is called __(14)__. Once the voltage has reached the rmp, it will still continue to decrease as these gates are notoriously slow to open. This results in a portion of the action potential that is more negative than the rmp called the __(15)__. The phase associated with this portion of the action potential is called __(16)__. Before returning to rmp, the active transport mechanisms called the __(17)___ will restore the ions back to their original locations.

Part III: Hyperkalemia (7 pts each question)

Juanita is a 58 year old female who felt the need to visit her doctor because of muscle cramping, weakness, and dizziness. In addition, Juanita was experiencing nausea, vomiting and diarrhea. In her medical history, Juanita had a history of diabetes mellitus and impaired renal function that was worsening. Her labs also reveal that she has a serum potassium level of 6.2 mEq/L. All other electrolytes measured within the normal ranges.

18. What is hyperkalemia? Be sure to reference the three fluid compartments (intracellular, extracellular and blood).

19. What effect does hyperkalemia have on the diffusion of K+ ions across the neuron’s membrane? Explain.

20. What effect does hyperkalemia have on the diffusion of Na+ ions across the neuron’s membrane? Explain.

21. What effect will hyperkalemia have on the rmp? Explain.

22. Let’s say Juanita’s issues are now with excessive blood sodium concentration called hypernatremia. What will the effect be on the rmp? Explain.

23. What effect will hypernatremia have on the generation of an action potential? Explain.

24. Finally, let’s examine hypercalcemia. What effects on neuromuscular transmission would you predict Juanita might experience? Explain.

Explanation / Answer

Answers:
1. Positive (Sodium Na+) ions

2. Negative ions

3. -70mv(millivolts)

4. Ion channels

5. Sodium ions

6. Potassium ions

7. Phosphatidyl serine, lyosomes, endosomes and Ionositol

PART -II

8. Sodium

9. Negative

10. Voltage gated sodium channels

11. Positive

12. Peak phase of depolarization

13. Potassium

14. Hyperpolarisation

15. Repolarisation

16. Relative refractory period

17. Sodium- Potassium pumps

18. Hyperkalaemia is increase in the levels of potassium in the serum. ECF K+ rises, ICF K+ decreases and blood it increase

19. It increases the resting membrane potential leading to depolarisation, increased excitability, prolonged refractory period. It is all due to the lesser negative value inside the cell membrane due to the efflux of K+ ions outside of the cell to the ECF and serum. So the resting membrane potential is now altered and it is near to the threshold value leading to more excitability

20. As potassium ions are effluxed already, less sodium ions are sufficient to initiate action potential. The variation in the potassium concentration gradient can lead to repolarization is delayed.

21. Hyperkalaemia makes the RMP to become less negative and brings the RMP closer to threshold value

22. It increases the RMP to become more positive due to more concentration gradient than usual

23. It increases the generation of action potential due to increased depolarisation

24. It also makes the RMP to become positive and favours Ca2+ influx. It causes synaptic plasticity, leading to lethargy, decreased excitability due to prolonged depolarization. Symptoms include headache, confusion, visual disturbance, poor memory and concentration. It may even lead to coma

20.

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