Adaptation in Vertebrate Photoreceptors

Abstract

When light is absorbed within the outer segment of a vertebrate photoreceptor, the conformation of the photopigment rhodopsin is altered to produce an activated photoproduct called metarhodopsin II or Rh(*). Rh(*) initiates a transduction cascade similar to that for metabotropic synaptic receptors and many hormones; the Rh(*) activates a heterotrimeric G protein, which in turn stimulates an effector enzyme, a cyclic nucleotide phosphodiesterase. The phosphodiesterase then hydrolyzes cGMP, and the decrease in the concentration of free cGMP reduces the probability of opening of channels in the outer segment plasma membrane, producing the electrical response of the cell. Photoreceptor transduction can be modulated by changes in the mean light level. This process, called light adaptation (or background adaptation), maintains the working range of the transduction cascade within a physiologically useful region of light intensities. There is increasing evidence that the second messenger responsible for the modulation of the transduction cascade during background adaptation is primarily, if not exclusively, Ca(2+), whose intracellular free concentration is decreased by illumination. The change in free Ca(2+) is believed to have a variety of effects on the transduction mechanism, including modulation of the rate of the guanylyl cyclase and rhodopsin kinase, alteration of the gain of the transduction cascade, and regulation of the affinity of the outer segment channels for cGMP. The sensitivity of the photoreceptor is also reduced by previous exposure to light bright enough to bleach a substantial fraction of the photopigment in the outer segment. This form of desensitization, called bleaching adaptation (the recovery from which is known as dark adaptation), seems largely to be due to an activation of the transduction cascade by some form of bleached pigment. The bleached pigment appears to activate the G protein transducin directly, although with a gain less than Rh(*). The resulting decrease in intracellular Ca(2+) then modulates the transduction cascade, by a mechanism very similar to the one responsible for altering sensitivity during background adaptation.

Electrical synapses between AII amacrine cells in the retina: Function and modulation

“…At the lowest light intensities (starlight, corresponding to scotopic vision), each rod will only capture a single photon perhaps once a minute, while at the highest intensities (daylight, corresponding to photopic vision), each cone may capture hundreds or even thousands of photons every second. Second, the sensitivity of the transduction process itself can be adjusted in response to changes in the ambient light intensity (reviewed by Fain et al, 2001). Third, rod and cone photoreceptors connect to two fundamentally different circuits in the retina: the rod and cone pathways ( Fig.…”

Why photoreceptors die (and why they don't)

“…This decrease plays an important role in light adaptation (see Ref. 23), but it may also be of fundamental importance in the life and death of the cell.…”

K+-Dependent Na+/Ca2+Exchangers: Key Contributors to Ca2+Signaling

“…NCKX1 is ideally suited for Ca 2+ extrusion under these conditions because its K + dependence provides an additional thermodynamic driving force to extrude Ca 2+ in the face of depolarized membrane potentials resulting from Ca 2+ and Na + influx through the cGMPgated channels. Illumination causes rhodopsin binding to and activation of the G-protein transducin, which in turn activates the membrane-bound cyclic nucleotide phosphodiesterase (PDE) (15). PDE catalyzes cGMP hydrolysis, resulting in the closure of the cGMP-gated channels.…”

“…Specialized photoreceptor guanylyl cyclases become activated by the reduced Ca 2+ concentration and resynthesize cGMP, which subsequently binds to and re-opens the cGMP-gated channels (23). The cGMP concentration, which is controlled by the Ca 2+ concentration, determines the open probability of the cGMP-gated channels to regulate the duration of the photoreceptor electrical response, a balance that is the basis of light adaptation (15).…”