Tetrodotoxin is a potent neurotoxin that blocks voltage gated sodium channels in neurons. When tetrodotoxin is present, what typically happens to the number of action potentials that can be generated?

Introduction / Context:
Action potentials are rapid electrical signals that travel along neurons and depend on the opening and closing of voltage gated ion channels. Tetrodotoxin, a toxin found in certain puffer fish, is famous for its ability to block voltage gated sodium channels. Understanding how this blockage affects the generation of action potentials is a classic question in neurophysiology and is important for appreciating how ion channel function underlies nerve signalling.

Given Data / Assumptions:

• Tetrodotoxin specifically blocks voltage gated sodium channels in the neuronal membrane.
• Action potentials require the rapid influx of sodium ions through these channels to depolarise the membrane.
• The question asks about changes in the number of action potentials that can be generated in the presence of tetrodotoxin.
• We assume typical experimental or physiological concentrations where channel blockade is substantial.

Concept / Approach:
In a normal neuron, an action potential begins when the membrane is depolarised to threshold, causing voltage gated sodium channels to open. Sodium ions rush into the cell, producing the rising phase of the action potential. If tetrodotoxin blocks these sodium channels, sodium cannot enter the neuron through them. As a result, the neuron cannot reach the threshold depolarisation needed to trigger an action potential, or the action potential is greatly reduced and fails to propagate. Therefore, the number of action potentials that can be generated decreases, often to zero if the block is strong enough.

Step-by-Step Solution:
Step 1: Recall that voltage gated sodium channels are essential for the rapid upstroke of the action potential in neurons. Step 2: When the membrane reaches threshold, these channels open and allow sodium ions to enter, causing a sharp depolarisation. Step 3: Tetrodotoxin binds to and blocks the pore of these sodium channels, preventing sodium from entering when the channels would normally open. Step 4: Without sufficient sodium influx, depolarisation cannot reach or maintain the threshold level needed to initiate or propagate an action potential. Step 5: As a result, the neuron either fails to fire action potentials at all or fires far fewer action potentials than under normal conditions. Step 6: Therefore, the number of action potentials decreases in the presence of tetrodotoxin.

Verification / Alternative check:
Experimental recordings from neurons treated with tetrodotoxin show that when the toxin is applied, the fast inward sodium current disappears and action potentials cannot be generated even when the membrane is stimulated. The membrane potential may still show small passive responses, but the characteristic spiking pattern is lost. These experimental observations support the conclusion that blocking sodium channels with tetrodotoxin reduces or abolishes action potentials rather than increasing their size or frequency.

Why Other Options Are Wrong:
The size (amplitude) of each action potential increases significantly is wrong because blocking sodium channels reduces, not enhances, the sodium current that produces the action potential upstroke. The number of action potentials increases due to enhanced sodium entry is incorrect because tetrodotoxin blocks sodium entry rather than enhancing it. The size of each action potential decreases but the frequency increases is also wrong because if the channels are blocked, both size and frequency of action potentials tend to fall, and in strong block conditions no action potentials are generated at all.

Common Pitfalls:
Some students focus only on the word toxin and guess that any property might change without thinking about the specific channel that is blocked. Others may confuse tetrodotoxin with agents that modulate potassium channels or with drugs that increase excitability. To avoid these mistakes, remember that tetrodotoxin is a sodium channel blocker and that sodium entry is essential for action potential initiation. Once you keep that causal link in mind, it becomes clear that the number of action potentials must decrease when sodium channels are blocked.

Final Answer:
The correct choice is The number of action potentials decreases, and may fall to zero as sodium channels are blocked, because tetrodotoxin prevents the sodium influx needed to generate normal action potentials.