Phototransduction in rod photoreceptors involves a cGMP-gated ion channel. In the dark state, high cGMP keeps the channel open and the cell is relatively depolarized (-40 mV). The molecular mechanism by which light absorption closes these channels is:
- A Activated rhodopsin (metarhodopsin II) activates transducin (Gαt) → PDE6 activation → cGMP hydrolysis → channel closure and hyperpolarization ✓
- B Light-activated rhodopsin directly blocks the cGMP-gated channel pore
- C Light activates adenylyl cyclase, increasing cAMP, which competes with cGMP for channel binding
- D Light-activated rhodopsin triggers Ca²⁺ influx that directly closes the cGMP-gated channel via calmodulin
Explanation
In the phototransduction cascade: (1) photon absorption isomerizes 11-cis-retinal to all-trans-retinal in rhodopsin → metarhodopsin II; (2) metarhodopsin II activates the heterotrimeric G-protein transducin (Gαt dissociates with GDP → GTP); (3) Gαt-GTP activates cGMP phosphodiesterase (PDE6) → cGMP hydrolyzed to 5'-GMP; (4) [cGMP] falls → cGMP-gated cation channels (CNG channels) close → reduced Na⁺ and Ca²⁺ influx → membrane hyperpolarizes → reduced glutamate release from rod synaptic terminal. Falling [Ca²⁺] i activates recoverin → regeneration of rhodopsin kinase sensitivity and guanylyl cyclase for adaptation.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.