Phototransduction in rod photoreceptors involves a G-protein cascade. In the dark, rods maintain a 'dark current.' The molecular mechanism maintaining the dark current is:

• A Constitutively active rhodopsin keeping cGMP phosphodiesterase inhibited → high cGMP → CNG channels open → Na+/Ca2+ influx (dark current)
• B Active Na+/K+-ATPase in the inner segment generating inward current through the outer segment
• C High Ca2+ in the dark keeping phosphodiesterase inhibited, maintaining cGMP and CNG channel opening
• D Guanylyl cyclase activity in the outer segment maintaining high cGMP levels → cyclic nucleotide-gated (CNG) channels remain open → depolarizing inward current (dark current) maintaining glutamate release ✓

Explanation

In the dark, guanylyl cyclase (GC) in the rod outer segment produces cGMP continuously, maintaining high cytoplasmic cGMP. cGMP binds to and holds CNG (cyclic nucleotide-gated) channels open on the outer segment membrane, allowing Na+ and Ca2+ influx (the depolarizing 'dark current'). This keeps the rod relatively depolarized (~-40mV) and glutamate release continuous (inhibitory to ON-bipolar cells). Light activation: photon absorbed by rhodopsin → conformational change (meta-rhodopsin II) → activates transducin (G-protein) → activates cGMP phosphodiesterase (PDE6) → hydrolyzes cGMP → CNG channels close → Na+/Ca2+ influx stops → hyperpolarization → reduced glutamate release → visual signal. Ca2+ has a feedback role (high dark Ca2+ inhibits GC; low light Ca2+ activates GC for recovery), but cGMP level maintenance is the primary mechanism.

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

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Written and medically reviewed by the StethoPrep medical team.