A motor nerve terminal is bathed in a solution containing tetrodotoxin at a concentration that abolishes voltage-gated sodium channels but leaves calcium channels functional. When the nerve is stimulated, what happens to neurotransmitter release at the terminal?

• A Release proceeds normally, since calcium entry is intact
• B Release is abolished because the action potential cannot invade the terminal ✓
• C Release is increased because sodium accumulation depolarizes the terminal
• D Only spontaneous miniature end plate potentials continue, at greatly reduced frequency

Explanation

Voltage-gated sodium channels generate the action potential that invades the nerve terminal. Without this invasion, voltage-gated calcium channels never open, and evoked transmitter release ceases entirely. Spontaneous quantal release continues at its baseline low frequency, which is independent of the action potential. Option A is wrong because calcium entry requires terminal depolarization by the invading spike. Option D is tempting but reverses the frequency change: miniaturized events persist at normal spontaneous frequency, only evoked release disappears.

Reference: Ganong's Review of Medical Physiology, 27th ed.

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Written and medically reviewed by the StethoPrep medical team.