Final answer:
The prediction was incorrect because TTX specifically targets voltage-gated Na+ channels, thus if R1 and R2 are unaffected by TTX, they may not be dependent on these sodium channels or do not bind TTX due to their structural differences.
Step-by-step explanation:
The prediction that TTX would block both receptors R1 and R2 was wrong because TTX specifically blocks voltage-gated Na+ channels. If R1 is unaffected by TTX, it suggests that R1 is not a voltage-gated sodium channel or has a different molecular structure that does not bind TTX. Similarly, if R2 is unaffected, it indicates that it also may not be a sodium channel impacted by TTX or it is not part of the neurons' action potential propagation system. The fourth option mentioned is not likely since it suggests a component is unaffected by TTX, which wouldn't explain why the prediction was wrong if that component deals with sodium channels.
The function of sodium channels is crucial because during an action potential, the depolarization reaches a threshold level, typically around -55mV, leading to the opening of these channels. The resulting influx of Na+ ions causes further depolarization. At the peak of the action potential, voltage-gated Na+ channels inactivate and cannot be opened for a brief period, known as the absolute refractory period. This ensures that the action potential propagates in one direction, towards the axon terminals.
If TTX were to block voltage-gated Na+ channels between R1 and the stimulus but R1 is unaffected, it suggests R1 operates independently of these channels. Similarly, if R2 is unaffected, it does not rely on sodium channels affected by TTX for its function either.