Rhodespin activation to signal pathway: The Human Visual System

The Photocascade

  • Again, the membrane potential of a RPC is controlled by conductances of K+ and Na+ ions whose transmembrane gradients are maintained by pumps.
    • In the dark, Na+ ions flow into the photoreceptor through nonselective cation channels that are activated by the second messenger cGMP.
    • Absorption of a photon triggers a biochemical cascade that lowers the concentration of cGMP, closing the gated channels and hyperpolarizing the cell to the K+ potential.


         
            B: T refers to transducin(the G-protein for rods). For (C) notice cones are less sensitive than rods as mentioned

Rhodopsin Activation

  • Rhodopsin is the visual pigment in rod cells.
    • Opsin component embedded in the disc membrane.
    • Retinal is the light-absorbing moiety.
      • 11-cis isomer covalently linked to a lysine residue of Opsin.
      • Absorption of a photon causes it to flip from 11-cis to the all-trans configuration.

Phosphodiesterase Activation through G-protein

  • The activated rhodopsin diffuses within the disc membrane where it encounters a G-protein (transducin in rods).
    • Inactive form binds GDP, but interaction with rhodopsin promotes binding of GTP instead.
    • This causes the alpha subunit of transducin to become activated (active subunit of transducin).
  • The active transducin subunit Tα-GTP complexes with cGMP phosphodiesterase (PDE), increasing its activity.
    • Enzyme hydrolyses cGMP → 5’-GMP
    • hence lowering cGMP concentration

Reduction of Inward Current

  • The concentration of cGMP controls the activity of the cGMP-gated Na+ channels in the plasma membrane of the outer segment.
    • With now Lowered cGMP from previously, the cGMP-gated Na+ channels close, reducing the inward current into the outer segment.

The Dark-Current

  • Dark current refers to the continuous inward and outward current in darkness.
    • PRC membrane potential \(\sim -40\) mV.
    • Cell’s synaptic terminal continually releases neurotransmitter glutamate.
  • No Na+ current flow (since cGMP-gated Na+ channels close as discussed above) in the presence of light. So in the light:
    • PRC membrane potential is now about that of potassium equilibrium potential \(\sim -70\) mV (since essentially now only K+ can pass through the cell) so it is essentially now hyperpolarized.
    • Hyperpolarization slows the release of glutamate from the photoreceptor terminal and so initiates a neural signal.

Summary

Dark

  • Rhodopsin (R) is inactive.
  • Transducin (T) (a G protein) remains in its inactive state.
  • Phosphodiesterase (PDE) enzyme is inactive.
  • Guanylate cyclase (GC) is producing cGMP.
  • High levels of cGMP keep the cGMP-gated Na+ channels open.
  • Na+ and Ca2+ ions enter the cell, keeping it depolarized.
  • Depolarization continuously releases glutamate, which inhibits the downstream bipolar cells.

Light

  • Photon activates rhodopsin (R), converting it into metarhodopsin II, which interacts with transducin (T).
  • Transducin (T) activates by exchanging GDP for GTP on its α-subunit.
  • The activated α-subunit of transducin binds to phosphodiesterase (PDE), activating it.
  • PDE breaks down cGMP into GMP, reducing cGMP levels.
  • Low cGMP levels cause the cGMP-gated Na+ channels to close.
  • No Na+ or Ca2+ influx, leading to hyperpolarization of the rod cell.
  • Reduced neurotransmitter (glutamate) release signals the presence of light.

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