A researcher applies a drug that specifically blocks voltage-gated potassium channels in neurons. What is the most likely effect on neural excitability?
BIncreased excitability — K⁺ channels normally repolarize the membrane, so blocking them prolongs depolarization and lowers threshold
CNo change — potassium channels only affect resting membrane potential, not excitability
DDecreased excitability — without K⁺ outflow, the membrane hyperpolarizes and becomes harder to fire
Voltage-gated K⁺ channels open after the peak of an action potential and allow K⁺ to flow out, repolarizing and hyperpolarizing the membrane — effectively applying the brake. Blocking these channels removes that brake: the membrane stays depolarized longer, recovery is delayed, and neurons can fire more readily or sustain firing more easily. Option D is wrong because blocking K⁺ outflow does not hyperpolarize the membrane — K⁺ wants to flow out at depolarized potentials (its equilibrium potential is negative), so blocking that outflow keeps the membrane more depolarized, not less.
Question 2 Multiple Choice
GABA-A receptors are ligand-gated ion channels that, when opened by GABA, allow Cl⁻ to flow into the neuron. Why does this reduce neural excitability?
ABecause Cl⁻ is positively charged and neutralizes the sodium influx from excitatory channels
BBecause Cl⁻ influx makes the interior of the neuron more negative, hyperpolarizing the membrane and moving it further from threshold
CBecause GABA channels compete for membrane space with sodium channels, physically blocking their opening
DBecause Cl⁻ ions inactivate voltage-gated Na⁺ channels by binding to their inactivation gates
Cl⁻ has a negative charge. When Cl⁻ flows in, the inside of the neuron becomes more negative (hyperpolarized). The action potential threshold is a specific membrane voltage (approximately −55 mV); hyperpolarizing the membrane moves it further away from that threshold, so a stronger excitatory stimulus is required to reach it. This is why GABA is the primary inhibitory neurotransmitter: opening GABA-A channels doesn't just fail to excite — it actively makes excitation harder. Benzodiazepines enhance this effect by prolonging GABA-A channel opening.
Question 3 True / False
Ion channels are passive pores that remain permanently open, simply allowing ions to diffuse freely down their concentration gradients.
TTrue
FFalse
Answer: False
Ion channels are gated — they switch between closed, open, and (for voltage-gated channels) inactivated states in response to specific stimuli. Voltage-gated channels open in response to membrane depolarization; ligand-gated channels open in response to neurotransmitter binding. Without gating, neurons could not control when ions cross the membrane, making action potentials and precise signaling impossible. The ability to open and close channels on timescales of milliseconds is what gives neurons their computational precision.
Question 4 True / False
The direction of ion flow through an open channel depends on both the concentration gradient and the electrical gradient across the membrane, not on concentration alone.
TTrue
FFalse
Answer: True
Ion movement is driven by the electrochemical gradient — the combined effect of the concentration gradient (diffusion) and the electrical potential gradient (electrostatic force). For example, Na⁺ is more concentrated outside the cell AND the inside is negatively charged, so both forces drive Na⁺ inward when Na⁺ channels open. For K⁺, the concentration gradient drives it out, but the negative interior partially opposes it. At the K⁺ equilibrium potential (~−90 mV), these forces exactly cancel and no net K⁺ flows despite the channel being open. The same ion can flow in either direction depending on conditions.
Question 5 Short Answer
Why is neural excitability better described as a dynamic balance of competing ionic conductances than as a fixed property of a neuron?
Think about your answer, then reveal below.
Model answer: Excitability is determined by which ion channels are open at any moment and how many. Voltage-gated Na⁺ channels increase excitability by depolarizing the membrane toward threshold. Voltage-gated K⁺ channels and inhibitory ligand-gated Cl⁻ channels reduce excitability by repolarizing or hyperpolarizing the membrane. These conductances change continuously: channel states respond to voltage, neurotransmitters, phosphorylation, and other factors. A neuron that fired easily a millisecond ago may be refractory now because Na⁺ channels are inactivated. The balance of conductances at any instant — not a fixed cellular parameter — determines excitability.
This dynamic view explains pharmacological interventions: drugs change excitability by tipping the balance. Lidocaine blocks Na⁺ channels (reduces excitability locally); seizure medications often enhance K⁺ or Cl⁻ conductances to counteract runaway depolarization. The concept of competing conductances is the universal framework for understanding why the same neuron can be highly excitable in one state and completely unresponsive in another.