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Resting Membrane Potential Simulation: Section 4

Significance of Resting Membrane Potentials and Related Case Studies

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The Significance of Resting Membrane Potentials.

If their resting membrane potentials deviate from their normal value, excitable cells become more or less responsive to stimuli that trigger action potentials.

A Brief Overview of Action Potentials.

An action potential is a momentary and sudden spike or reversal in the membrane potential that serves as an electrochemical signal.

  • This process begins when a stimulus causes the cell membrane to depolarize to a threshold level, typically around -55 mV.
  • The change in membrane potential activates (opens) sodium (Na+) voltage-gated channels embedded in the membrane.
  • As a result, Na+ ions flow into the cell through the channels, and the membrane potential rapidly depolarizes.
  • When the membrane potential reaches approximately +30 mV, the Na+ channels self-inactivate (close), while potassium (K+) channels open.
  • The rapid outward flow of K+ ions through the channels repolarizes the membrane.
  • Na+ channels revert to their original resting state when the membrane returns to its normal resting potential, allowing the process to begin again.

Channel States During An Action Potential

Channel states during an action potential

Review Questions.

Question 1: What is an action potential?

Question 2: What event triggers the start of an action potential?

Question 3: What causes the rapid rise in membrane potential?

Question 4: When do the Na+ channels inactivate (close)?

Question 5: What causes the membrane to repolarize?

Question 6: When do all of the Na+ channels revert to their original resting state?

What Factors Cause the Resting Membrane Potentials to Deviate from Its Normal Value?

Changes in ion concentrations or variations in membrane permeability can cause the resting membrane potential to become either more or less polarized. If the membrane potential becomes more negative (hyperpolarized), it would require a higher-intensity stimulus to initiate an action potential. Conversely, lower-intensity stimuli would trigger an action potential if the membrane potential becomes less negative (depolarized).

Review Question.

Question 1: Would an excitable cell be more or less sensitive to stimuli if its resting membrane potential becomes less polarized than normal?

How Can the Resting Membrane Potential Affect Na+ Channel Reactivation?

During an action potential, the cell membrane must fully repolarize to its normal resting potential for the Na+ channels to return to their resting conformation (shape) after becoming inactivated. If the membrane remains partially depolarized for extended periods, many Na+ channels may not activate (open) when stimulated. This condition reduces membrane excitability, causing muscle weakness or paralysis.

Review Question.

Question 1: What may happen if an excitable cell membrane does not fully repolarize while producing action potentials?

Case Studies

1. Exercise-Induced Hyperkalemia

Case Subject:

An experienced female 41-year-old marathon runner has been preparing for an upcoming race. She is healthy and trains by running several miles every other day.

Signs and Symptoms:

After a particularly long and intense training session, the subject began experiencing muscle weakness and heart arrhythmias.

Diagnosis:

After her transport to the hospital, the subject’s blood tests revealed her potassium level had risen to 7.0 mmol/l. She was diagnosed with hyperkalemia, a condition characterized by high levels of potassium in the blood.

Usually, the potassium levels in an individual’s blood and extracellular fluid are 3.5-5.3 mmol/l, and severe manifestations typically occur when the serum potassium concentration is ≥ 7.0 mmol/l.

Female runner, hyperkalemia case study subject

Due to the action of the Na+/K+ pump (ATPase), the skeletal muscles contain about 80% of the intracellular potassium. Prolonged high-intensity endurance exercises can cause skeletal muscle cells to break down (rhabdomyolysis), causing the release of potassium into extracellular fluid.

Treatment:

The subject was given 5 units of insulin and 25g of glucose (to avoid low blood sugar or hypoglycemia), a standard treatment for hyperkalemia. The insulin increases the activity of the Na+/K+ pump proteins (ATPases).

Case Study Analysis.

Question 1: Why would the subject’s extracellular K+ level increase if many of her skeletal muscle cells ruptured during exercise?

Question 2: The subject’s potassium level rose to 7.0 mmol/l. How does this potassium concentration affect the resting membrane potential of the subject’s muscle cells? Use the GHK calculator below to determine the answer.

Question 3: Does the change in resting membrane potential make the subject’s skeletal muscle cells more or less polarized?

Question 4: Why did the magnitude of membrane polarization change?

Question 5: Why did the subject’s skeletal muscle cells become fatigued?

Question 6: How did the administration of insulin help lower the extracellular potassium level?

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2. Exercise-Associated Hyponatremia  (EAH)

Case Subject:

Another runner, a middle-aged male, has been training for the same marathon. He is in good health but new to endurance running.

The subject has gradually increased his exercise times to improve his endurance for the upcoming race.

He completed a half marathon at his top pace during his latest training session. It was a hot day, so he drank a large volume of regular water while running.

Signs and Symptoms:

After his run, the subject began to feel weak, dizzy, and confused.

Male runner, hyponatremia case study subject

Diagnosis:

The subject was taken to the local hospital, where his blood results showed a sodium level of 125 mmol/l. He was diagnosed as having Exercise-Associated Hyponatremia (EAH), a condition that occurs when the blood sodium concentration decreases to less than 135 mmol/l.

The likely cause for the subject’s drop in blood sodium concentration was his overconsumption of hypotonic (low electrolyte) fluids, sodium lost in sweat, and an elevated level of ADH (antidiuretic hormone). In response to intense exercise, the level of ADH increases to maintain body fluids by promoting water reabsorption by the kidneys.

Treatment:

The subject was given 150 mL of hypertonic 3% saline (NaCl solution) to offset his low blood sodium.

Case Study Analysis.

Question 1: How did the subject’s hyponatremia change the resting membrane potential of his muscle and nerve cells? Use the GHK calculator below to determine the answer.

Question 2: Would the change in resting membrane potential make the subject’s muscle and nerve cells more or less responsive to activating stimuli?

Question 3: Would the change in resting membrane potential be a likely cause of the subject’s signs and symptoms?

Question 4: What factor limits the impact of the subject’s hyponatremia (low blood sodium) on resting membrane potentials?

Question 6: Could the change in water balance disrupt the functions of nerve tissues encased by the skull and cause the subject’s signs and symptoms? (Reference: NIH – “Click here.)

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