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makes rapid control of gain on the basis of signals from single rods
impossible in night vision. Thus, the authors point out that less
than 0.1 photon is absorbed per second per rod under so-called low
to moderate scotopic light intensity levels and that, therefore, the
rod system has to exploit spatially averaging of impulses from many
rods in order to adapt rapidly to a change in light intensity at these
levels.
The authors found behaviour measurements supporting the
suggestion that at least one adaptation mechanism that may control
the gain of rod-mediated signals operated in the rod bipolar pathways.
In accordance with this suggestion, they could conclude from their
own physiological recordings that the synapses between rod bipolar
and AII amacrine cells were key gain-control sites at low light levels.
These sites, they argued, would provide a unique opportunity for
specialized processing operating exclusively on rod signals.
Yet, the review article of Dunn and Rieke ( 2006 ) leaves us
with the impression that research on visual sensitivity regulation
is still at a rather undeveloped stage. Obviously, much remains to
be clarified. Thus, the different roles in sensitivity regulation played
by the different types of receptor, horizontal, bipolar, amacrine and
ganglion cells, and also by cells central to the retina, are still largely
unknown. Indeed, in spite of the great effort to reveal the gain-control
mechanisms of light and dark adaptation at the very first ion channels
in the visual pathway (the cGMP gated channels in the plasma
membrane of the outer segment of the receptors), there is at present
no general agreement about these sensitivity-regulation mechanisms.
A deeper understanding would require more knowledge about how
dark and light adaptation change the amount of cGMP that gates
the outer segment channels and how these changes are related to
sensitivity measured psychophysically. The picture appears extremely
complicated, since evidence indicates that retinoids (all-trans retinal,
all-trans retinol and 11-cis retinal), phosphorylation enzymes and
Ca 2+ -binding proteins all may modulate the sensitivity (Dean et al .,
2002 ; McCabe et al ., 2004 ). Knowledge of such influences are, of
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