The dark current in photoreceptors (rods) is maintained in the dark by which mechanism, and what happens when light strikes the photoreceptor?

• A In dark: cGMP keeps cGMP-gated cation channels OPEN, causing depolarization and tonic glutamate release; light: rhodopsin activation → transducin → PDE6 activates → cGMP hydrolyzed → channels CLOSE → hyperpolarization → reduced glutamate release ✓
• B In dark: Na+ channels are closed, the rod is hyperpolarized, no glutamate release; light causes depolarization and glutamate release
• C In dark: voltage-gated Ca2+ channels open, causing Ca2+ influx and glutamate release; light hyperpolarizes via Ca2+ channel closure
• D Dark current is maintained by K+ influx through leak channels; light activates K+ efflux causing depolarization

Explanation

In darkness, high intracellular cGMP keeps cyclic nucleotide-gated (CNG) cation channels open, allowing Na+ and Ca2+ influx — the 'dark current' — which depolarizes the rod to about −40 mV, causing tonic glutamate release from the synaptic terminal. Light absorption by rhodopsin activates transducin (Gt protein), which activates phosphodiesterase-6 (PDE6), hydrolyzing cGMP → GMP. Falling cGMP closes CNG channels, hyperpolarizing the rod to ~−70 mV, reducing then stopping glutamate release. This is the phototransduction cascade — a G protein-mediated second messenger system.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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