Fred Rieke

Light Adaptation in Salamander L-Cone Photoreceptors

Cones, which are the dominant photoreceptors in the eye in daylight, operate over a
range of over one million in mean light intensity. In order to encode this wide range
of visual inputs cones must adjust their sensitivity, or adapt, to large changes in
illumination. In this experiment the researchers used suction electrodes to record
from individual salamander cones as they responded to step changes in
illumination. They found that light initially suppressed circulating current, which
then partially recovered (sagged) over several seconds. After light onset the
sensitivity of the cone to dim flashes decreased rapidly, approaching a minimum of
500ms. They also found that background light didnt affect the rising phase of the
dim flash response (according to the article this is a measure of initial gain of
phototransduction). When light was extinguished, circulating current was seen to
overshoot its level in darkness. During this period the sensitivity of the cone
required several seconds to recover. Using previous theory the authors suggest 3
mechanisms for the sag, overshoot, and slow recovery of sensitivity. The
phototransduction cascade is slowly inactivated during the light step, residual
activity remains after the step has been extinguished, and an increase in guanylate
cylase activity during the light step persists after the light is extinguished.
The thing I notice most about this paper is that it seems to assume some previous
knowledge on the area, so a lot of it is a bit out of my depth. For example I dont
really know what guanylate cylase is, other than an enzyme. This made it a bit
difficult to puzzle out the details, but the big, take home message ended up being
fairly ordinary. They basically found that three already known mechanisms do what
one would expect them to do given changes in light intensity, resulting in their sag,
overshoot, recovery model. Thats not to say its not an important paper, just not
extraordinarily exciting one. I wonder how much this contributes to the delay in
human eyes as a whole adjusting to different light levels. The pupil has to adjust its
size to changes in light intensity, so I guess the question would be, which is the
limiting factor?

Presentation
Dr. Riekes presentation used the retina as an example of parallel processing. There
are effectively 2 paths that lead to ON ganglion cells. The first is the rod bipolar
pathway which comes from, unsurprisingly, the rods. The second, the cone bipolar
pathway, come from the cones. The rod bipolar pathway meets the cone bipolar
pathway through an electrical connection at ON cone bipolar cells. The end result of
this is that the pathway can be completed when cones or rods are active, but
information will take a different route. Lower light levels actually results in the cells
responding linearly while high light is non-linear. Increasing light will overall

decrease the tonic output from the rod bipolar pathway, allowing the input from the
cone bipolar pathway to be more dominant and cells to respond more nonlinearly. I
would be interested to learn what other processes in the brain use this convergent
parallel processing. From what Dr. Rieke said it seems fairly common. In the retina
this process results in altering between linear/nonlinear responses. Is this the same
effect in the rest of the brain? Dr. Rieke also mentioned there is an early electrical
connection between the two pathways. It seemed like in the retina this didnt have
much of an effect on parallel processing, but in other areas perhaps this crossing
over between parallel processes is important. On this subject, Id also like to know
exactly what this earlier electrical connection does if it doesnt affect parallel
processing. Overall an interesting lecture that presented, in a fairly easy to
understand area, a mechanism involved in very complex processes.