Lidocaine apparently blocks voltage-gated sodium channels in sensory neurons and thus prevents action potentials, but photoreceptors like rod cells require hyperpolarization (through blockage of its sodium channels) for the neurotransmitter to be released / generator potential set up, so would adding lidocaine to the retinal cells stimulate them? Would it hypothetically make us think there's light even when it's dark?
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See Wikipedia for an overview of the signal transduction that occurs in photoreceptor cells.
Briefly, light results in increases in cGMP; cGMP binds a cGMP-gated sodium channel (not a voltage-gated sodium channel) causing the channel to close. Therefore, light -> less sodium entry.
Lidocaine blocks a different type of sodium channel: the fast voltage-gated sodium channels involved in neurotransmission. It's possible there is some cross-reactivity, but it would be entirely coincidental as it's from a completely different family of channels.
In any event, the retina has all sorts of other neuron types: bipolar cells, retinal ganglion cells, and various interneuron types, that all communicate with each other through action potentials mediated by voltage-gated sodium channels. If you were to apply lidocaine to the retina, you'd lose all this neurotransmission.
answered Oct 21, 2022 at 15:08
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1$\begingroup$ the last paragraph really hit the nail, I feel like I should've realized that before. $\endgroup$– RayanCommented Oct 21, 2022 at 15:47
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1$\begingroup$ @Rayan Good, but paragraphs 2 and 3 are probably more important to the specific question asked here: it's important to recognize that there are different types of channels that conduct the same ions, this will come up in a lot more situations. $\endgroup$– Bryan Krause ♦Commented Oct 21, 2022 at 16:58