In phototransduction, when a photon is absorbed by rhodopsin in a rod photoreceptor, the cell hyperpolarises rather than depolarises. Which sequence of events explains this paradoxical hyperpolarisation?
- A Activated rhodopsin (metarhodopsin II) activates transducin (Gt), which activates PDE6, hydrolysing cGMP; cGMP-gated cation channels close; Na⁺ and Ca²⁺ entry ceases; K⁺ efflux via open K⁺ channels hyperpolarises the cell ✓
- B Photon absorption activates rhodopsin, which directly opens Cl⁻ channels, causing Cl⁻ influx and hyperpolarisation
- C Activated rhodopsin inhibits guanylate cyclase, reducing cGMP; cGMP-gated Na⁺ channels open in the dark are ligand-gated and close when cGMP falls, causing hyperpolarisation
- D Photon energy is transduced into a H⁺ gradient by opsin-linked proton pumps, acidifying the cytoplasm and activating inward-rectifier K⁺ channels
Explanation
Phototransduction: Rhodopsin → (photon) → Metarhodopsin II → activates Gt (transducin) → activates phosphodiesterase-6 (PDE6) → rapidly hydrolyses cGMP → [cGMP]i falls → cGMP-gated non-selective cation channels (CNG channels, which were held open in the dark by cGMP) close → Na⁺ and Ca²⁺ influx ceases while K⁺ continues to exit through open K⁺ leak channels → net hyperpolarisation (from ~-40 mV in dark to ~-70 mV in light). This reduces glutamate release from the rod terminal onto bipolar cells. Option C incorrectly states that rhodopsin inhibits guanylate cyclase; that is a recovery mechanism (GC activation by GCAP after Ca²⁺ falls). PDE6 activation, not GC inhibition, is the primary event.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.