Phototransduction

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Phototransduction is the conversion of a stimulus from electromagnetic radiation into a cellular effect. The conversion of a light stimulus into a receptor potential as a physiological signal in sensory cells is also called photoelectric transduction . The process sequence taking place in the photoreceptors of the retina of the eye can be referred to as a visual signal transduction cascade .

Structure of the receptor cells

Schematic representation of the photoreceptor cell. The discs are shown in yellow.

Light entering the eye hits the rhodopsin , which is contained in the disk membranes in high concentrations (approx. 30,000 molecules / µm²). Disks are flat, tightly packed vesicles inside the outer segment of the receptor cell. They arise as folds in the outer segment membrane. In rods, these folds are detached from the plasma membrane. They are there as a stack of discs in the outer segment. They are retained with tenons.

The process of phototransduction mainly takes place in the outer segments of the photoreceptor cells (adjacent figure). A number of membrane-bound and soluble proteins are involved in this. Rhodopsin, a G-protein-coupled receptor , and a guanylate cyclase are stored in the disk membranes . The soluble proteins involved are transducin , a heterotrimeric G protein , and a cGMP - phosphodiesterase . In addition, cGMP-controlled Na + / Ca 2+ channels and Na + / K + exchangers are located in the plasma membrane of the outer segments. The inner segment contains the cell nucleus, the mitochondria as well as Na + / K + -ATPases , a Na + / Ca 2+ -Antiporter and potassium channels and is responsible for the metabolism of the cell.

Signal transduction process

The signal transduction cascade

Schematic representation of visual signal transduction. Here the area outlined in red in the “
Photoreceptor ” illustration is shown enlarged (not to scale).

The exact process is shown in the adjacent figure:

  1. The incident light is absorbed by 11-cis-retinal, which is bound to the opsin via a Schiff base bond in the hydrophobic interior of the opsin (rhodopsin is a combination of opsin and 11-cis-retinal). The 11-cis retinal isomerizes to the all-trans retinal. The rhodopsin is then activated through several intermediate states. The activated rhodopsin (called metarhodopsin II) then binds the alpha subunit of the transducin .
  2. This binding induces the exchange of GDP for GTP in the α-subunit of the transducin . This further leads to the β / γ subunit dissociating and the α subunit becoming active.
  3. The α-subunit of the transducin cleaves the two γ-subunits of the cGMP phosphodiesterase (PDE) , binds them and thus activates the PDE. Splitting off a γ subunit would lead to partial activation of the PDE.
  4. The active PDE now splits cGMP into GMP. The falling cGMP level inhibits the influx of cations into the cell. The falling Ca 2+ concentration now activates the guanylyl cyclase-activating enzyme, which in turn activates guanylyl cyclase. As a result, cGMP is now also rebuilt, so there is a balance between build up and breakdown.
  5. After some time, the intrinsic GTPase of the α-subunit splits the GTP into GDP and phosphate. This releases the γ subunits of the PDE again.
  6. The thus regenerated α-subunit now reassembles with the β / γ-subunit and forms the original transducin complex.
  7. The γ subunits bind again to the phosphodiesterase and thus inactivate it. Therefore, no more cGMP is broken down, the ion channels for Ca 2+ and Na + remain open and cause a repolarization of the membrane (see below).

Regeneration of the system

Activated rhodopsin (also metarhodopsin II) breaks down after a while into its protein component opsin and all-trans-retinal. The latter is converted back into 11-cis-retinal with an isomerase, which can then bind again to opsin. However, this process takes too long. Therefore, rhodopsin is inactivated and regenerated via the following reaction sequence: Rhodopsin is phosphorylated by a rhodopsin kinase. Arrestin now binds to the phosphorylated rhodopsin . Dephosphorylation of the opsin by a Ca 2+ -sensitive phosphatase leads to the dissociation of the arrestin, whereupon the rhodopsin can now be regenerated with 11-cis-retinal. The arrestin-mediated inactivation prevents activated rhodopsin from maintaining the signal cascade for too long.

Arrestin also plays a role in the light-dark adaptation of the eye, as the phosphorylation and thereby the arrestin-mediated inactivation of rhodopsin increases with the strength and duration of a light stimulus.

The concentration of cGMP is regulated via the Ca 2+ level.

As already mentioned above, there is also a feedback control loop via the Ca 2+ level in the cell (Fig. “ Signal transduction ” and opposite), which is also involved in the regeneration and adaptation of these processes. If the ion channels are closed, no more Ca 2+ flows into the cell and the constantly active Ca 2+ exchanger transports Ca 2+ out of the cell, so that the Ca 2+ concentration drops. This causes an increase in the activity of the guanylyl cyclase-activating enzyme (GCAP) (also: guanylate cyclase-activating enzyme), which is inhibited by Ca 2+ ions. GCAP now activates a cGMP-synthesizing guanylyl cyclase and the low cGMP level is brought back to the old level. Na + -Ca 2+ channels open again through the cGMP and the Ca 2+ level rises again, whereby the activity of GCAP and at the same time also the guanylyl cyclase decrease again, etc. So a cGMP equilibrium arises from the breakdown by the cGMP-PDE and the synthesis of cGMP by guanylyl cyclase.

The resulting impulse can also be regulated via the Ca 2+ level and thus contributes to the adaptation to light conditions (e.g. through pH-dependent Ca 2+ channels). Once the light stimulus has passed, however, the activity of the PDE stops relatively quickly through the regeneration of transducin (from section d to section a in Fig. “ Signal transduction ”). The guanylyl cyclase now synthesizes cGMP, so that its concentration increases again to the normal level. This also reactivates the cGMP-dependent cation transporter and the dark current flows again. The Ca 2+ level also rises again and indirectly stops guanylyl cyclase. The system is ready for the next light pulse.

Signal forwarding

In the dark, the neurotransmitter glutamate is continuously released in the photoreceptors. In cones, this has an inhibitory effect on the horizontal and ON bipolar cells , but activates the OFF bipolar cells via different glutamate receptors (ON-OFF dichotomy ). The closure of the cation channels in the cell membrane of the photoreceptor and the subsequent hyperpolarization prevent the neurotransmitter glutamate from being released any further. As a result, the inhibiting ion channels of the horizontal and bipolar cells are closed. This allows action potentials to arise again in the ganglion cells. This is the actual electrical signal that is modulated in the retina and then passed on to the visual center of the brain .

See also

Individual evidence

  1. Stefan Silbernagl , Agamemnon Despopoulos : Pocket Atlas Physiology . 8th edition. Thieme Verlag, 2012, ISBN 978-3-13-567708-8 , p. 370.
  2. Werner Müller, Stephan Frings: Animal and human physiology: an introduction . Springer-Verlag, 2009, ISBN 978-3-642-00462-9 , p. 509.
  3. Christopher Moyes, Patricia Schulte: Animal Physiology . Pearson, 2008, ISBN 978-3-8273-7270-3 , p. 312.
  4. a b Georg Löffler, Petro E. Petrides, Peter C. Heinrich: Biochemistry and Pathobiochemistry . S. 686. Springer Medizin Verlag, Heidelberg, 2006. ISBN 3-540-32680-4 .
  5. ^ Jan C. Behrends, Josef Bischofberger, Rainer Deutzmann: Physiology. ISBN 3131384123 . P. 648.