Final answer:
An action potential is still recorded at R1 despite voltage-gated Na+ channels being blocked between R1 and R2 with TTX because the Na+ channels between the stimulus and R1 are unaffected, allowing depolarization and the generation of an action potential at R1.
Step-by-step explanation:
When voltage-gated Na+ channels between R1 and R2 are blocked with tetrodotoxin (TTX), an action potential is still recorded at R1 because the voltage-gated Na+ channels between the stimulus and R1 are unaffected by the TTX. In the process of generating an action potential, a stimulus initially causes depolarization of the membrane. This depolarization opens the voltage-gated Na+ channels, leading to a rapid increase of the membrane potential as Na+ flows into the neuron. This results in the action potential rising to about +40 mV. When the membrane potential approaches its peak, voltage-gated K+ channels also open, allowing K+ to flow out, which leads to repolarization of the neuron. The timing is such that Na+ channels inactivate and do not allow more Na+ into the cell during this phase. The action potential is an all-or-nothing event and travels as a wave along the axon. Thus, any segment of the axon where Na+ channels are not blocked by TTX can initiate an action potential, given that it is depolarized to the threshold potential of about -55 mV. Since the area between R1 and the stimulus is not affected by TTX, action potentials generated there can still be recorded at R1.