It is amazing how our eyes adapt to let us see in hugely differing light conditions, from almost complete darkness to blinding sunlight. It is almost as if they had built-in sunglasses. Two papers in today's issue of Neuron provide striking insights into the molecular nature of this important phenomenon, with converging experimental evidence from work in rats and flies.
The first step in “seeing” happens in the eye. It is there that light hits the specialized photoreceptor cells of the retina and is captured by complexes of proteins that convert the captured light energy into an electrical signal that is ultimately carried to the brain.
As one might expect, these light-sensing protein complexes typically sit at the outer edges of the photoreceptors in the most advantageous position for capturing light.
What two research teams have found is that when there is very bright light, some of the proteins in these light-sensing complexes actually move away from the edges of the cell to the inside of the cell, where they are no longer able to detect the light.
Thus, although there may be lots of light around, there are fewer complexes left on the edges of the cells to capture it and as a result, the response is kept from becoming too big.
Conversely, in very dim light, all the proteins move back out to the outer edges, which increases the number of functional complexes that are there to capture the limited light.
Therefore, altering the number of protein complexes available to respond to light in different light conditions is one of the tricks the eye has developed to allow us to see well in a wide range of light, from very dim light to bright sunlight.
In the rat retina, a research team led by Vadim Arshavsky at Harvard has discovered that light causes transducin, one of the proteins in the complex and a component of the "molecular cascade" that turns light into nerve impulses, to become internalized inside the receptor cells.
Since less transducin is available, the transformation of light into electrical impulses won't occur as efficiently.
Similarly, Huber and colleagues at Universität Karlsruhe in Germany, using the power of fruit fly genetics, reveal that another one of the proteins critical for converting light energy into an electrical signal, the ion channel protein TRPL, also shuttles from the surface of the receptor cells, where it normally resides when it is dark, to a storage compartment when the light is bright.
(Reference: Neuron, Volume 34 Number 1, March 28, 2002)
[Contact: Vadim Y. Arshavsky, Armin Huber]
28-Mar-2002
