All questions
Question 1
A neuron rested at -70 mV; which ion was most linked to that negativity?
- K+ movement through leak channels (correct answer)
- Ca2+ movement through voltage-gated channels
- Na+ movement out of the cell during depolarization
- Cl- pumping by the Na+/K+ pump
Explanation: This question tests understanding of membrane potential basics and ion gradients in introductory anatomy and physiology. Membrane potential is the voltage difference across a cell membrane resulting from differential ion concentrations, primarily sodium and potassium. For example, neurons use the resting membrane potential to trigger action potentials. Choice A is correct because K+ movement through leak channels primarily contributes to the negative potential. Choice B is incorrect because Ca2+ channels are not open at rest. To help students, focus on visualizing ion concentrations inside and outside the cell and use models to demonstrate the pump's role. Encourage practice with diagrams illustrating ion movements and potential changes.
Question 2
A neuron rested at -70 mV; what did the negative sign indicate?
- Inside was negative compared with outside (correct answer)
- Outside was negative compared with inside
- Na+ concentration was higher inside than outside
- K+ concentration was higher outside than inside
Explanation: This question tests understanding of membrane potential basics and ion gradients in introductory anatomy and physiology. Membrane potential is the voltage difference across a cell membrane resulting from differential ion concentrations, primarily sodium and potassium. For example, neurons use the resting membrane potential to trigger action potentials. Choice A is correct because the negative sign indicates the inside is negative relative to the outside. Choice C is incorrect because Na+ is higher outside, not inside. To help students, focus on visualizing ion concentrations inside and outside the cell and use models to demonstrate the pump's role. Encourage practice with diagrams illustrating ion movements and potential changes.
Question 3
A neuron had Na+ high outside and K+ high inside; what best described resting potential?
- Inside was negative relative to outside (correct answer)
- Inside was positive relative to outside
- Inside and outside had the same charge
- Resting potential depended only on Ca2+ channels
Explanation: This question tests understanding of membrane potential basics and ion gradients in introductory anatomy and physiology. Membrane potential is the voltage difference across a cell membrane resulting from differential ion concentrations, primarily sodium and potassium. For example, neurons use the resting membrane potential to trigger action potentials. Choice A is correct because the inside of the neuron is negative relative to the outside due to ion gradients and selective permeability. Choice B is incorrect because it suggests a positive interior, which occurs during depolarization, not rest. To help students, focus on visualizing ion concentrations inside and outside the cell and use models to demonstrate the pump's role. Encourage practice with diagrams illustrating ion movements and potential changes.
Question 4
A neuron had high Na+ outside; what did that gradient tend to do at rest?
- Drive Na+ into the cell when channels were open (correct answer)
- Drive Na+ out of the cell when channels were open
- Drive K+ into the cell when channels were open
- Prevent any ion movement across the membrane
Explanation: This question tests understanding of membrane potential basics and ion gradients in introductory anatomy and physiology. Membrane potential is the voltage difference across a cell membrane resulting from differential ion concentrations, primarily sodium and potassium. For example, neurons use the resting membrane potential to trigger action potentials. Choice A is correct because the high external Na+ gradient drives Na+ into the cell when channels open. Choice B is incorrect because the gradient drives Na+ in, not out. To help students, focus on visualizing ion concentrations inside and outside the cell and use models to demonstrate the pump's role. Encourage practice with diagrams illustrating ion movements and potential changes.
Question 5
During an action potential, voltage-gated Na⁺ channels open when the membrane potential reaches approximately -55 mV. If a neuron's resting potential is -70 mV and the Na⁺ equilibrium potential is +60 mV, what primarily determines whether the neuron will reach threshold for action potential generation?
- The magnitude of depolarizing current must exceed the capacity of K⁺ leak channels to maintain resting potential (correct answer)
- The intracellular Na⁺ concentration must increase sufficiently to shift the equilibrium potential past threshold
- The membrane resistance must decrease to allow faster equilibration between inside and outside ion concentrations
- The voltage-gated Na⁺ channels must undergo conformational changes that lower their activation threshold below -70 mV
- The extracellular K⁺ concentration must decrease to make the K⁺ equilibrium potential more negative than threshold
Explanation: When you encounter action potential questions, focus on the fundamental competition between depolarizing and repolarizing forces that determines whether threshold will be reached.
To generate an action potential, the membrane must depolarize from -70 mV to -55 mV. This requires depolarizing current (usually from synaptic inputs or stimuli) to overcome the neuron's natural tendency to stay at rest. At resting potential, K⁺ leak channels continuously allow K⁺ to flow out, maintaining the negative interior. For threshold to be reached, incoming depolarizing current must be strong enough to overpower this K⁺ efflux and drive the membrane potential upward by 15 mV.
Choice A correctly identifies this principle - the depolarizing current must exceed the repolarizing capacity of K⁺ leak channels.
Choice B misunderstands equilibrium potentials. The Na⁺ equilibrium potential (+60 mV) is fixed by concentration gradients and doesn't need to "shift past threshold." Small changes in intracellular Na⁺ during normal signaling barely affect this equilibrium potential.
Choice C incorrectly suggests that decreasing membrane resistance helps reach threshold. Lower resistance would actually make it harder to achieve the voltage changes needed for threshold by allowing charges to dissipate more easily.
Choice D proposes that Na⁺ channels change their activation threshold, but channel properties are fixed - they always open at approximately -55 mV. The channels don't adapt their threshold to the resting potential.
Remember: Action potential generation is about current balance, not voltage alone. Always consider what forces are competing when the membrane potential changes.
Question 6
A student measures the membrane potential of a muscle cell and finds it to be -90 mV. The cell is then treated with ouabain, which blocks the Na⁺/K⁺-ATPase pump. Over the next several minutes, the membrane potential gradually changes to -60 mV and stabilizes. What does this experiment demonstrate about the original -90 mV potential?
- The original potential was maintained entirely by the electrogenic Na⁺/K⁺ pump, which directly contributes -30 mV to the membrane potential
- The original potential reflected steady-state balance between pump activity and passive leak currents, with pump failure allowing Na⁺/K⁺ gradients to dissipate (correct answer)
- The original potential was an artifact of measurement error, and -60 mV represents the true equilibrium potential for this cell type
- The pump blockade activated compensatory ion channels that depolarized the cell to maintain ionic homeostasis at a new set point
- The original potential required ATP-dependent maintenance of Cl⁻ gradients, which collapsed when cellular energy was depleted by pump inhibition
Explanation: When you encounter membrane potential questions involving pump inhibitors, focus on understanding the dynamic balance between active transport and passive ion movement that maintains resting potential.
The Na⁺/K⁺-ATPase pump actively maintains steep concentration gradients by pumping 3 Na⁺ out for every 2 K⁺ in, consuming ATP. Meanwhile, ions constantly leak back down their gradients through various channels. The resting potential reflects the steady-state balance between this active pumping and passive leakage.
When ouabain blocks the pump, active transport stops but passive leakage continues. Na⁺ continues entering the cell while K⁺ exits, gradually dissipating the concentration gradients. As these gradients weaken, the driving force for ion movement decreases until a new equilibrium is reached at -60 mV. This demonstrates that the original -90 mV required continuous pump activity to counteract ongoing leak currents.
Choice A incorrectly suggests the pump directly contributes a fixed voltage. While the pump is electrogenic (moves net positive charge out), its primary role is maintaining gradients that determine membrane potential. Choice C misinterprets the results as measurement error rather than recognizing a real physiological change. Choice D incorrectly invokes compensatory mechanisms that don't exist in this scenario.
Remember: resting membrane potential isn't static but represents dynamic equilibrium. When you see pump inhibitor experiments, think about how removing active transport allows gradients to dissipate, revealing the pump's essential role in maintaining the cell's electrical state.
Question 7
A pharmaceutical researcher is testing a novel compound that selectively blocks K⁺ leak channels in neurons. When applied to a neuron with a normal resting potential of -70 mV, the compound causes the membrane potential to shift to -45 mV within seconds. What does this result suggest about the role of K⁺ leak channels in membrane potential maintenance?
- K⁺ leak channels contribute -25 mV to the resting potential through their electrogenic transport activity independent of concentration gradients
- K⁺ leak channels normally provide the dominant hyperpolarizing influence, and their blockade unmasks depolarizing influences from other ion channels (correct answer)
- K⁺ leak channels are primarily responsible for action potential repolarization, and their blockade prevents the cell from returning to rest
- K⁺ leak channels regulate intracellular K⁺ concentration, and their blockade rapidly alters the K⁺ equilibrium potential by 25 mV
- K⁺ leak channels control membrane capacitance, and their blockade changes the electrical properties that determine steady-state potential
Explanation: When you encounter questions about membrane potential and ion channels, focus on how different channels work together to establish and maintain the resting potential. The resting membrane potential results from a delicate balance between various ion movements across the membrane.
In this experiment, blocking K⁺ leak channels caused the membrane potential to shift from -70 mV to -45 mV (a 25 mV depolarization). This dramatic change reveals that K⁺ leak channels normally provide a strong hyperpolarizing influence by allowing K⁺ to flow out of the cell down its concentration gradient. When these channels are blocked, other ion movements (particularly Na⁺ influx through leak channels) become more dominant, causing depolarization. This confirms that answer B is correct - K⁺ leak channels provide the dominant hyperpolarizing influence, and blocking them unmasks depolarizing influences from other channels.
Answer A is wrong because K⁺ leak channels aren't electrogenic pumps; they're passive channels that move ions down concentration gradients. Answer C incorrectly describes action potential repolarization - while K⁺ channels are important for repolarization, leak channels primarily maintain resting potential, not repolarization kinetics. Answer D misunderstands the timeframe and mechanism - altering intracellular K⁺ concentration enough to shift the equilibrium potential by 25 mV would take much longer than seconds and require massive ion movement.
Remember: Resting potential reflects the balance of all ion movements. K⁺ leak channels typically dominate this balance, making the inside negative. When studying membrane physiology, always consider how blocking one pathway reveals the contributions of others.
Question 8
A patient's blood work shows hyponatremia (low plasma Na⁺ = 125 mM) compared to normal (140 mM), while intracellular Na⁺ remains at normal levels (15 mM). How would this condition most likely affect the Na⁺ equilibrium potential and neuronal excitability?
- Na⁺ equilibrium potential becomes less positive, reducing the driving force for Na⁺ influx and decreasing excitability (correct answer)
- Na⁺ equilibrium potential becomes more positive, increasing the driving force for Na⁺ influx and increasing excitability
- Na⁺ equilibrium potential remains unchanged because intracellular Na⁺ concentration is normal, so excitability is unaffected
- Na⁺ equilibrium potential becomes less positive, but excitability increases due to reduced membrane stability from ionic imbalance
- Na⁺ equilibrium potential becomes more negative, creating a larger gradient that enhances action potential amplitude and excitability
Explanation: When you encounter questions about electrolyte imbalances and neuronal function, focus on how changes in ion concentrations affect equilibrium potentials and the driving forces for ion movement.
The sodium equilibrium potential (E_Na) is determined by the Nernst equation: ENa=FRTln[Na+]in[Na+]out. With hyponatremia reducing extracellular Na⁺ from 140 mM to 125 mM while intracellular Na⁺ remains at 15 mM, the concentration gradient decreases. This makes E_Na less positive (closer to zero).
During action potentials, the driving force for Na⁺ influx depends on the difference between the membrane potential and E_Na. When E_Na becomes less positive, this driving force weakens, meaning less Na⁺ enters during depolarization. This reduces the amplitude and speed of action potentials, decreasing neuronal excitability.
Option A correctly identifies both effects: E_Na becomes less positive and excitability decreases due to reduced driving force. Option B incorrectly states E_Na becomes more positive—this would only occur if extracellular Na⁺ increased or intracellular Na⁺ decreased. Option C wrongly assumes that unchanged intracellular Na⁺ means no effect on E_Na, ignoring the critical role of the extracellular concentration. Option D correctly identifies the less positive E_Na but incorrectly claims increased excitability—reduced ionic gradients don't cause hyperexcitability through "membrane instability."
Remember: equilibrium potentials depend on concentration ratios across the membrane. Always consider both sides of the equation when analyzing electrolyte disorders and their effects on cellular excitability. Question 9
A research laboratory is studying membrane potentials in neurons bathed in different ionic solutions. In Solution A, the membrane potential is -70 mV. When switched to Solution B with identical ionic concentrations except for doubled extracellular Cl⁻ concentration, the membrane potential changes to -85 mV. What can be concluded about this neuron's membrane permeability?
- The membrane has significant permeability to Cl⁻, and Cl⁻ contributes substantially to the resting potential through electrochemical equilibrium (correct answer)
- The membrane is impermeable to Cl⁻, and the potential change results from altered Na⁺/K⁺ pump activity due to ionic strength changes
- The membrane has low Cl⁻ permeability, and the potential change results from osmotic effects that alter cell volume and ion concentrations
- The membrane becomes more permeable to Cl⁻ only when extracellular Cl⁻ increases, indicating voltage-gated Cl⁻ channel activation
- The membrane has equal permeability to all ions, and the potential change reflects the new equilibrium of all ionic gradients combined
Explanation: When you encounter questions about membrane potential changes in response to altered ionic concentrations, think about the Goldman-Hodgkin-Katz equation and how permeable ions contribute to resting potential based on their concentration gradients and membrane permeability.
The key observation here is that doubling extracellular Cl⁻ made the membrane potential more negative (from -70 mV to -85 mV). Since Cl⁻ is negatively charged, this hyperpolarization indicates that Cl⁻ is moving according to its electrochemical gradient and significantly influencing the membrane potential. When extracellular Cl⁻ doubles, the equilibrium potential for Cl⁻ becomes more negative (using the Nernst equation: ECl=−61log[Cl−]in[Cl−]out). If the membrane is permeable to Cl⁻, this shift in Cl⁻ equilibrium potential will drive the overall membrane potential toward this new, more negative value.
Choice A correctly identifies that significant Cl⁻ permeability allows Cl⁻ to contribute substantially to resting potential through electrochemical equilibrium. Choice B is wrong because if the membrane were impermeable to Cl⁻, changing its concentration wouldn't affect membrane potential directly. Choice C incorrectly attributes the change to osmotic effects rather than electrochemical driving forces. Choice D wrongly suggests voltage-gated channel activation, but the potential change occurs immediately upon solution switch, indicating constitutive permeability rather than voltage-dependent gating.
Remember: if changing an ion's concentration alters membrane potential in the predicted direction, that ion must have significant membrane permeability and contribute to the resting potential. Question 10
During patch-clamp experiments, a researcher observes that when a membrane patch is held at different voltages, the current through Na⁺ channels varies. At -70 mV, there is no net Na⁺ current even when channels are open. At -40 mV, there is strong inward Na⁺ current. At +60 mV, there is no net current. What explains this pattern?
- Na⁺ channels are voltage-gated and only open between -40 mV and +60 mV, with maximum conductance at intermediate potentials
- The driving force for Na⁺ movement depends on the difference between membrane potential and Na⁺ equilibrium potential, creating current reversal at ENa (correct answer)
- Na⁺ channel selectivity changes with voltage, allowing Na⁺ influx at negative potentials but blocking it at positive potentials
- The concentration gradient for Na⁺ is voltage-dependent, with effective gradients only existing at intermediate membrane potentials
- Na⁺ channels undergo conformational changes that reverse their selectivity from inward to outward current flow at depolarized potentials
Explanation: When analyzing ion channel currents in patch-clamp experiments, you need to understand that current flow depends on both channel conductance and the driving force for ion movement. The driving force is determined by the difference between the membrane potential and the ion's equilibrium potential.
The pattern described reveals the Na⁺ equilibrium potential (ENa). At -70 mV, even though channels are open, there's no net current because this voltage is below the threshold where the electrochemical gradient favors Na⁺ movement. At -40 mV, the membrane potential is sufficiently depolarized relative to ENa to create a strong driving force for Na⁺ influx. At +60 mV, you're at or very close to ENa itself, so there's no net driving force—this is the reversal potential where current equals zero regardless of channel opening.
Answer B correctly identifies that current depends on the driving force relationship between membrane potential and ENa. Answer A incorrectly suggests voltage-gated opening kinetics explain the current pattern, but the question states channels are already open at -70 mV. Answer C wrongly claims that channel selectivity changes with voltage—Na⁺ channels maintain their selectivity regardless of membrane potential. Answer D incorrectly suggests concentration gradients are voltage-dependent, when in reality the gradients remain constant while the electrical driving force changes.
Remember: in electrophysiology questions, always consider both whether channels are open AND whether there's a driving force for ion movement. Current requires both channel availability and an electrochemical gradient.
Question 11
In a resting neuron, which ion gradient most strongly drove diffusion into the cell?
- K+ gradient drove K+ into the cell
- Na+ gradient drove Na+ into the cell (correct answer)
- Cl- gradient drove Cl- out of the cell
- Ca2+ gradient drove Ca2+ out of the cell
Explanation: This question tests understanding of membrane potential basics and ion gradients in introductory anatomy and physiology. Membrane potential is the voltage difference across a cell membrane resulting from differential ion concentrations, primarily sodium and potassium. For example, neurons use the resting membrane potential to trigger action potentials. Choice B is correct because the Na+ gradient, with high Na+ outside, strongly drives Na+ diffusion into the cell. Choice A is incorrect because the K+ gradient drives K+ out, not in. To help students, focus on visualizing ion concentrations inside and outside the cell and use models to demonstrate the pump's role. Encourage practice with diagrams illustrating ion movements and potential changes.
Question 12
A membrane patch contains only voltage-gated potassium channels. When the membrane potential is held at -40 mV (above threshold), these channels open and K+ flows out of the cell. If the extracellular K+ concentration is gradually increased while maintaining the membrane potential at -40 mV, what will happen to the magnitude of potassium current?
- Current magnitude will decrease and eventually reverse direction as the driving force for K+ movement decreases and then changes sign (correct answer)
- Current magnitude will increase proportionally because higher extracellular K+ creates a larger concentration gradient favoring efflux
- Current magnitude will remain constant because the membrane potential is voltage-clamped and channel conductance is unchanged
- Current magnitude will initially decrease then plateau at zero when extracellular K+ matches the voltage-clamp potential
Explanation: When analyzing ion channel behavior, you need to understand that current depends on both channel conductance and the driving force for ion movement. The driving force is determined by the difference between the membrane potential and the ion's equilibrium potential.
Initially, with normal extracellular K+ concentrations, the K+ equilibrium potential is around -90 mV. Since the membrane is held at -40 mV, there's a strong driving force (50 mV difference) pushing K+ out of the cell, creating outward current. However, as you increase extracellular K+, the equilibrium potential becomes less negative (moves toward 0 mV) according to the Nernst equation. This reduces the driving force for K+ efflux, decreasing current magnitude. Eventually, when extracellular K+ is high enough that the equilibrium potential reaches -40 mV, there's no driving force and current becomes zero. Further increases would make the equilibrium potential more positive than -40 mV, reversing the driving force and causing K+ to flow into the cell.
Option B incorrectly assumes higher extracellular K+ increases efflux, ignoring how this change affects the equilibrium potential. Option C misunderstands that voltage-clamping maintains membrane potential but doesn't prevent changes in driving force as ion gradients shift. Option D suggests current would plateau at zero, missing that further increases in extracellular K+ would reverse current direction.
Remember: current equals conductance times driving force. Even with constant conductance, changing ion gradients alter the equilibrium potential and thus the driving force for current flow. Question 13
A resting neuron had many K+ leak channels; what did that mainly affect?
- It made the membrane potential more negative (correct answer)
- It made the membrane potential more positive
- It eliminated the Na+ concentration gradient
- It stopped ATP use by the Na+/K+ pump
Explanation: This question tests understanding of membrane potential basics and ion gradients in introductory anatomy and physiology. Membrane potential is the voltage difference across a cell membrane resulting from differential ion concentrations, primarily sodium and potassium. For example, neurons use the resting membrane potential to trigger action potentials. Choice A is correct because many K+ leak channels allow more K+ outflow, making potential more negative. Choice B is incorrect because that would depolarize the membrane. To help students, focus on visualizing ion concentrations inside and outside the cell and use models to demonstrate the pump's role. Encourage practice with diagrams illustrating ion movements and potential changes.
Question 14
A neuron had a resting potential; what feature was required to create it?
- Unequal ion concentrations and selective permeability (correct answer)
- Equal ion concentrations and no membrane proteins
- Only Ca2+ channels and no Na+/K+ pump
- Only Na+ channels open and K+ channels closed
Explanation: This question tests understanding of membrane potential basics and ion gradients in introductory anatomy and physiology. Membrane potential is the voltage difference across a cell membrane resulting from differential ion concentrations, primarily sodium and potassium. For example, neurons use the resting membrane potential to trigger action potentials. Choice A is correct because unequal concentrations and selective permeability create the potential. Choice B is incorrect because equal concentrations would eliminate potential. To help students, focus on visualizing ion concentrations inside and outside the cell and use models to demonstrate the pump's role. Encourage practice with diagrams illustrating ion movements and potential changes.
Question 15
A neuron has an intracellular K+ concentration of 140 mM and an extracellular K+ concentration of 5 mM. If the membrane becomes selectively permeable to K+ only, and the equilibrium potential for K+ is calculated to be -85 mV, what would happen to the membrane potential if the extracellular K+ concentration suddenly increased to 15 mM?
- The membrane potential would become more negative because the concentration gradient for K+ efflux increases significantly
- The membrane potential would become less negative because the driving force for K+ efflux decreases with reduced gradient (correct answer)
- The membrane potential would remain at -85 mV because only intracellular K+ concentration determines the equilibrium potential
- The membrane potential would reverse polarity to positive because extracellular K+ now drives influx against the original gradient
Explanation: According to the Nernst equation, the equilibrium potential depends on the ratio of ion concentrations across the membrane. When extracellular K+ increases from 5 mM to 15 mM, the concentration gradient decreases (from 140:5 to 140:15), making the equilibrium potential less negative (closer to zero). This reduces the driving force for K+ efflux. Choice A is wrong because a smaller gradient means less efflux, not more. Choice C incorrectly suggests only intracellular concentration matters. Choice D is wrong because the gradient still favors efflux, just less so. Question 16
Refer to the diagram. A neuron's membrane potential is being recorded while the extracellular K⁺ concentration is systematically varied. Based on the relationship shown, what does the slope of this line indicate about the membrane's ionic permeability?
- The membrane is selectively permeable to K⁺ only, as evidenced by the theoretical Nernst slope of 58 mV per 10-fold concentration change
- The membrane has mixed permeability to multiple ions, with K⁺ being dominant but not exclusive based on the slope being less than theoretical maximum (correct answer)
- The membrane permeability changes with K⁺ concentration, indicating voltage-gated K⁺ channels that open at higher concentrations
- The membrane is primarily permeable to Na⁺ and Cl⁻, with K⁺ having minimal influence on the potential despite concentration changes
- The membrane shows equal permeability to K⁺ and Na⁺, creating a compromise potential that varies linearly with K⁺ concentration
Explanation: The slope of membrane potential vs. log[K⁺]out indicates the relative contribution of K⁺ to the resting potential. A pure K⁺ electrode would show a 58 mV change per 10-fold [K⁺] change (Nernst slope). A slope less than 58 mV indicates mixed permeability - K⁺ is influential but other ions (Na⁺, Cl⁻) also contribute to the potential, reducing K⁺'s dominance. Choice A incorrectly assumes pure K⁺ selectivity. Choice C incorrectly invokes voltage-gated channels rather than passive permeability. Choice D incorrectly dismisses K⁺ influence despite the clear relationship shown. Choice E incorrectly describes equal K⁺/Na⁺ permeability.
Question 17
Two cells, A and B, have identical intracellular ion concentrations but different membrane permeabilities. Cell A has a resting potential of -80 mV and is primarily permeable to K+. Cell B has a resting potential of -50 mV and has mixed permeability to K+, Na+, and Cl−. If both cells are treated with ouabain (which blocks the Na-K pump), what will happen to their membrane potentials over time?
- Both cells will depolarize at the same rate because they have identical intracellular starting conditions and pump inhibition effects
- Cell A will depolarize faster because it has a larger initial driving force for Na+ influx when pump activity ceases
- Cell B will hyperpolarize initially because pump inhibition reduces intracellular Na+, then gradually depolarize as gradients dissipate
- Cell A will remain stable longer because its membrane potential depends mainly on the K+ gradient, which changes slowly without the pump (correct answer)
Explanation: When you encounter questions about membrane potential and pump inhibition, focus on how different membrane permeabilities affect a cell's dependence on active transport versus passive gradients.
Cell A's membrane potential of -80 mV reflects its high K+ permeability - it's close to the K+ equilibrium potential (around -90 mV). This means Cell A's resting potential is primarily determined by the K+ concentration gradient, which is naturally maintained by the large difference between intracellular and extracellular K+ concentrations. When ouabain blocks the Na-K pump, this K+ gradient will dissipate slowly because the pump normally moves only small amounts of K+ relative to the total intracellular pool.
Cell B's mixed permeability creates a membrane potential that's a weighted average of multiple ion equilibrium potentials. Its -50 mV potential indicates significant Na+ permeability, making it more dependent on active pump maintenance. Without the pump, Na+ influx will quickly alter the membrane potential.
Answer A is wrong because identical starting conditions don't matter when membrane permeabilities differ dramatically. Answer B incorrectly suggests Cell A will change faster, when its K+-dominated potential provides more stability. Answer C misunderstands pump inhibition - blocking the pump doesn't initially reduce intracellular Na+; it prevents Na+ removal, leading to accumulation.
The correct answer is D. Remember: cells with high K+ permeability are more resistant to pump inhibition because their membrane potential relies primarily on the large, slowly-changing K+ gradient rather than active transport. Question 18
During an action potential, the membrane potential reaches +30 mV while the Na+ equilibrium potential is +60 mV and the K+ equilibrium potential is -90 mV. At this peak moment, what is the primary factor preventing the membrane potential from reaching the Na+ equilibrium potential?
- The sodium channels begin rapid inactivation while potassium channels start opening, creating competing ionic currents that limit depolarization (correct answer)
- The concentration gradient for sodium becomes depleted as too many sodium ions enter the cell during the rising phase
- The membrane becomes equally permeable to all ions, creating a mixed potential that averages all equilibrium potentials together
- The sodium-potassium pump activates immediately to counteract sodium influx and prevent excessive depolarization beyond +30 mV
Explanation: At the peak of an action potential, voltage-gated sodium channels begin to inactivate while voltage-gated potassium channels start to open. This creates opposing currents: continued (but decreasing) sodium influx and increasing potassium efflux. The membrane potential represents the balance of these currents, not the equilibrium potential of any single ion. Choice B is wrong because the concentration gradients don't significantly change during a single action potential. Choice C incorrectly describes equal permeability. Choice D is wrong because the Na-K pump is too slow to affect action potential dynamics.
Question 19
A student is studying nerve conduction in a laboratory setting. She isolates a nerve fiber and measures its properties under different ionic conditions. In the normal physiological solution, the nerve has a resting potential of -70 mV. She then performs a series of manipulations to understand ion gradients and membrane potential.
The student replaces the normal extracellular solution with one containing high K+ (50 mM instead of 5 mM) and low Na+ (50 mM instead of 145 mM). She observes that the resting potential changes to -20 mV and the nerve can no longer generate normal action potentials. What is the primary reason action potentials fail in this condition?
- The sodium equilibrium potential becomes too negative to provide sufficient driving force for rapid depolarization during action potential initiation
- The altered potassium gradient eliminates the repolarization mechanism necessary for action potential recovery and return to baseline
- The depolarized resting potential causes chronic inactivation of voltage-gated sodium channels, preventing them from opening during stimulation (correct answer)
- The reduced electrochemical gradient for potassium prevents adequate hyperpolarization needed to reset the membrane for subsequent action potentials
Explanation: When you encounter questions about action potential failure, focus on how ionic conditions affect both resting potential and channel behavior. The key insight here is understanding voltage-gated sodium channel inactivation.
The high K+ solution shifts the resting potential from -70 mV to -20 mV because potassium's equilibrium potential becomes less negative (closer to 0). This drastically depolarized resting potential creates a critical problem: voltage-gated sodium channels have two gates—an activation gate and an inactivation gate. At normal resting potentials around -70 mV, the inactivation gates remain open and ready. However, when the membrane sits at -20 mV chronically, these inactivation gates close and stay closed, making the channels unavailable for opening even when stimulated. This is why action potentials fail—the sodium channels simply cannot participate in depolarization.
Option A is incorrect because while the sodium equilibrium potential does change, it's still positive enough to drive depolarization if channels could open. Option B misses the mark—potassium can still repolarize the membrane; the issue isn't with repolarization mechanisms. Option D focuses on hyperpolarization for "resetting," but the fundamental problem occurs before any action potential even begins.
The correct answer is C because chronic depolarization inactivates sodium channels, preventing normal excitability.
Remember this pattern: when resting potential becomes too depolarized (usually above -55 mV), think about sodium channel inactivation as the primary cause of excitability loss, not just changes in driving forces or repolarization mechanisms. Question 20
A student measures the equilibrium potential for Cl− in a muscle cell and finds it to be -70 mV, which exactly matches the resting membrane potential. She concludes that chloride ions do not contribute to the resting potential. Later, she blocks chloride channels with a specific inhibitor and observes that the resting potential becomes less stable and more variable. What explains this apparent contradiction?
- Chloride channels were actually contributing to membrane potential, but the equilibrium potential measurement was inaccurate due to technical limitations
- The chloride channel blocker has off-target effects on other ion channels, creating the observed instability rather than true chloride effects
- Blocking chloride channels indirectly affects sodium-potassium pump activity, which then destabilizes the membrane potential through altered gradients
- Even though chloride is at equilibrium, chloride channels provide membrane conductance that stabilizes potential against small perturbations from other ions (correct answer)
Explanation: When you encounter questions about ion channels and membrane potential, remember that an ion can be at equilibrium while still playing an important stabilizing role through its conductance properties.
The key insight here is distinguishing between driving force and conductance. Since chloride's equilibrium potential (-70 mV) matches the resting potential, there's no net driving force for Cl− movement under steady-state conditions - the student's initial conclusion seems logical. However, chloride channels still provide membrane conductance that acts like a "buffer" against voltage fluctuations.
Think of it like a shock absorber: when other ions cause small voltage perturbations, chloride channels allow rapid Cl− movement that counteracts these changes and pulls the membrane back toward -70 mV. Without this stabilizing conductance, the membrane becomes more susceptible to voltage "noise" from other ion movements.
Option A incorrectly assumes measurement error, but -70 mV equilibrium potentials for chloride are physiologically normal in muscle cells. Option B suggests off-target effects, but specific chloride channel blockers are well-characterized tools that primarily affect chloride conductance. Option C proposes indirect effects on the sodium-potassium pump, but pump activity typically isn't significantly altered by chloride channel blockade in the short term.
Study tip: Remember that ions at equilibrium can still be functionally important. Always consider both the magnitude of driving force (determines net ion flow) and conductance (determines how effectively an ion can respond to voltage changes). This distinction appears frequently in neurophysiology questions.