Phototransduction in rod photoreceptors involves a G-protein cascade. In darkness, what is the state of the rod cell and how does light change it?
- A In darkness: cell is hyperpolarized and releases GABA. Light causes depolarization and increased glutamate release to signal bipolar cells
- B In darkness: high cGMP keeps cGMP-gated cation channels open, cell is depolarized (~−40 mV), and glutamate is continuously released. Light activates rhodopsin → transducin → phosphodiesterase → cGMP hydrolysis → channel closure → hyperpolarization → decreased glutamate release ✓
- C In darkness: Na⁺/K⁺ ATPase is inactive; light activates it, generating hyperpolarization
- D In darkness: rhodopsin is fully activated, maintaining photoreceptor in a refractory state; light causes rhodopsin inactivation and channel opening
Correct answer: B. In darkness: high cGMP keeps cGMP-gated cation channels open, cell is depolarized (~−40 mV), and glutamate is continuously released. Light activates rhodopsin → transducin → phosphodiesterase → cGMP hydrolysis → channel closure → hyperpolarization → decreased glutamate release
Explanation
Rod photoreceptors are depolarized in darkness due to the dark current: cGMP holds cGMP-gated Na⁺/Ca²⁺ channels open, maintaining the membrane at about −40 mV and sustaining tonic glutamate release onto bipolar cells. Upon photon absorption, retinal isomerizes (11-cis to all-trans), activating rhodopsin → transducin (Gα) → phosphodiesterase 6 → cGMP hydrolysis → channel closure → hyperpolarization → reduced glutamate release. This sign-inverting neurotransmitter change encodes the light signal.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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