Interactive Neuron Action Potential Lab
Anatomy & Physiology: Neural Signaling and Clinical Applications
Open the PhET Simulation
Click the link below to open the Neuron simulation in a new tab. Keep both this page and the simulation open so you can follow along with the procedure.
Open PhET Neuron SimulationLab Objectives
- • Observe and describe the sequence of events during an action potentialA rapid, temporary electrical charge that travels along neurons, allowing signal transmission.
- • Identify the roles of sodium(Na⁺): Major ECF cation; important for fluid balance, nerve function. and potassium(K⁺): Major ICF cation; essential for muscle and nerve function. ionsCharged atoms or molecules. in neural signaling
- • Understand how voltage-gated channelsProtein passages in the cell membrane that allow specific molecules to pass through. respond to membrane potential changes
- • Connect action potential physiologyThe study of how the body functions. to clinical scenarios involving electrolyte imbalances
Simulation Procedure
Explore the Resting State
When you first open the simulation, the neuron is at rest. Look at the membrane and observe the distribution of ions.
- • Enable “Show Charges” and “Show Concentrations” options
- • Observe which ions are more concentrated inside vs outside
- • Notice the charges on each side of the membrane
- • Look at the voltage reading on the voltmeter
Question 1:
What is the resting membrane potential? Which ion has a higher concentration inside the cell, and which has a higher concentration outside?
Stimulate the Neuron
Click the “Stimulate Neuron” button and watch what happens. You may want to slow down the simulation speed to observe more carefully.
- • Watch the voltage graph as the action potential occurs
- • Observe the movementA fundamental property of life involving motion of the body or its parts. of ions across the membrane
- • Pay attention to which channels open first
- • Note the color changes in the voltage-gated channels
Question 2:
Describe the sequence of events you observed. Which ions moved first? What happened to the membrane potential?
Examine the Depolarization Phase
Stimulate the neuron again and pause during the rising phase (depolarizationThe loss of electrical charge across a membrane, triggering an action potential.) of the action potential.
- • Which voltage-gated channels are open?
- • What color are the sodium channels?
- • Which direction are sodium ions moving?
- • Is the inside of the cell becoming more positive or negative?
Question 3:
Why do sodium ions rush INTO the cell during depolarization? What is driving this movement? (Hint: Consider both concentration and electrical gradients)
Observe Repolarization
Continue the simulation and pause during the falling phase (repolarizationThe return of membrane potential to a negative value after depolarization.).
- • What has happened to the sodium channels?
- • Which channels are now open?
- • Which ions are moving and in which direction?
- • What is happening to the membrane potential?
Question 4:
Explain why potassium ions leave the cell during repolarization. How does this restore the negative membrane potential?
Identify the Refractory Period
Try to stimulate the neuron again immediately after an action potential completes.
- • Can you trigger another action potential right away?
- • Look at the sodium channel states
- • Notice if there’s a brief period of hyperpolarizationAn increase in membrane potential, making the inside of the neuron more negative.
- • Try stimulating at different times during recovery
Question 5:
What is the refractory period and why does it exist? What would happen if neuronsThe functional cells of the nervous system that transmit signals. could fire action potentials continuously without a refractory period?
Examine the Sodium-Potassium Pump
Look for the sodium-potassium pumpA transport protein that moves sodium out of the cell and potassium into the cell using ATP. (Na⁺/K⁺-ATPase) in the simulation. It’s usually shown as a rotating or animated pump structure.
- • Watch the pump work continuously
- • How many sodium ions does it move out?
- • How many potassium ions does it move in?
- • Does it work during or after the action potential?
Question 6:
The sodium-potassium pump moves 3 Na⁺ out and 2 K⁺ in, and it requires ATPThe energy currency of cells used for muscle contraction. energyThe capacity to do work or cause change.. Why is this pump essential for maintaining the resting potential? What would happen if the pump stopped working?
Simulation Complete!
Once you’ve completed all steps and answered the questions, move to the Case Study tab to apply what you’ve learned to a real clinical scenario.
Clinical Case Study
A Critical Situation in the Operating Room
The Patient
Mrs. Chen, a 58-year-old woman, is scheduled for an elective knee replacement surgery. She has a history of chronic kidney disease (Stage 3) but has been cleared for surgery. Her pre-operative bloodwork shows a serum potassium level of 5.8 mEq/L (normal range is 3.5-5.0 mEq/L), which is elevated but not critical enough to delay surgery after consultation with nephrology.
The Anesthesia Plan
The anesthesiologist plans to use general anesthesia with succinylcholine as the neuromuscular blocking agent to facilitate rapid intubation. Succinylcholine is a depolarizing muscle relaxant that works by binding to acetylcholine receptorsProteins on the motor end plate of the sarcolemma that bind acetylcholine to trigger contraction. at the neuromuscular junctionThe connection between a motor neuron and a muscle fiber., causing sustained depolarization of the muscle membrane.
Key Point: Succinylcholine causes muscle cellsThe basic structural and functional units of life. to release potassium into the bloodstream as they depolarize.
In a typical patient, this increases serum K⁺ by about 0.5 mEq/L, but in patients with certain conditions or pre-existing hyperkalemiaHigh potassium levels in the blood., the increase can be much more dangerous.
The Complication
Shortly after administering succinylcholine, the cardiac monitor shows peaked T-waves and widening of the QRS complex, which are classic ECG signsObjective clinical findings observable by a provider (e.g., edema, fever). of hyperkalemia. The patient’s potassium level has risen to approximately 6.5 to 7.0 mEq/L. The surgical team must act quickly to prevent cardiac arrest.
Why is this dangerous?
Elevated extracellular potassium affects the resting membrane potential of ALL excitable cells, including cardiac myocytes and neurons. This disrupts normal electrical signaling throughout the body.
Treatment Protocol
The anesthesiologist immediately initiates hyperkalemia treatment:
- Calcium gluconate IV: Stabilizes cardiac membranes (doesn’t lower K⁺ but protects the heart)
- Insulin with glucoseA simple sugar that is the main source of energy for cells. IV: Drives K⁺ back into cells by activating the Na⁺/K⁺-ATPase pump
- Albuterol nebulizer: Beta-agonist that stimulates cellular uptake of potassium
- Sodium bicarbonate(HCO₃⁻) – A crucial buffer in blood that helps maintain pH balance; formed when carbon dioxide: Alkalinizes blood, promoting K⁺ shift into cells
After 15 minutes of treatment, the ECG normalizes and the patient stabilizes. Surgery is postponed until Mrs. Chen’s potassium can be better controlled medically through dietary modifications and possible adjustment of her medications.
Case Study Analysis
Use your understanding from the PhET simulation to answer these questions about Mrs. Chen’s case.
Clinical Application Questions
List of terms
- head
- action potential
- sodium
- potassium
- ions
- channels
- physiology
- movement
- depolarization
- repolarization
- hyperpolarization
- neurons
- sodium-potassium pump
- ATP
- energy
- acetylcholine receptors
- neuromuscular junction
- cells
- hyperkalemia
- signs
- glucose
- bicarbonate
- concentration gradient
- threshold
- excitability
- sensory neurons
- electrolyte balance
- hypoxia