Final answer:
Lidocaine applied to the retina would likely cause hyperpolarization of retinal cells due to the blockage of voltage-gated sodium channels, impairing neurotransmitter release and signal transduction, leading to potential visual disturbances.
Step-by-step explanation:
If lidocaine was applied to the retina, the hypothetical outcome would likely be C) Lidocaine's action would cause hyperpolarization in retinal cells, leading to reduced neurotransmitter release and impaired signal transduction. Lidocaine acts by blocking voltage-gated sodium channels. In the context of retinal function, blocking these channels would prevent sodium ions from entering the retinal cells, which is essential for the depolarization phase of action potential generation.
Normally, photoreceptors in the retina undergo tonic activity, which means they have a baseline firing rate in the dark due to a resting release of the neurotransmitter glutamate. Light exposure hyperpolarizes these cells and reduces the glutamate release onto bipolar cells, thereby altering the signal that is sent to the brain. However, if lidocaine were to block the sodium channels, photoreceptors might become further hyperpolarized, mimicking a state of darkness and thus preventing proper signal transmission to the brain.
This impact would likely result in a failure to correctly transmit visual information, causing visual disturbances or loss of vision until the effects of the drug wear off. Consequently, lidocaine's function as a local anesthetic in numbing sensory perception would translate in the retina to an inhibition of normal visual processing.