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Study discovers mechanism by which the two interact

(HealthDay is the new name for HealthScoutNews.)

MONDAY, July 28, 2003 (HealthDayNews) -- Researchers working with rats have discovered the mechanism by which the brain uses sensory input to create proper vision, accounting for phenomena first seen 44 years ago.

In 1959, Drs. David H. Hubel and Torsten N. Wiesel made the groundbreaking discovery that the proper development of the visual cortex depended on visual experience in early life.

When Hubel and Wiesel covered one eye in kittens, they found the brain's cortex would cease to respond to stimulation of that eye and the animal would become blind in that eye. In 1981 they were awarded the Nobel Prize in Medicine for their work.

However, the biological mechanisms that account for this phenomenon have remained a mystery until now. In new research, Dr. Mark Bear, a professor of neuroscience at the Massachusetts Institute of Technology in Cambridge, and his colleagues have uncovered that mechanism.

In earlier experiments, Bear's team found that lack of stimulation to the retina was not the cause. "It was really that lack of visual activity that was causing a change in the cortex," he says.

When animals are very young, the development of proper vision requires precise wiring of input from both eyes, Bear adds.

Working with animal brain cells, they found a molecular mechanism at work that causes weakening of vision. This mechanism, called long-term depression (LTD), results in the loss of neurotransmitters in synapses of brain cells and eventually the permanent loss of the synapse between the axon and dendrite, Bear notes.

LTD is the long-term depression of synaptic transmission. LTD has been shown to operate in many different types of synapses of the brain, he adds.

In the experiments reported in the August issue of Nature Neuroscience, the researchers have taken their work one step further and found in young rats that had one eye covered, LTD had the same effect they had noted in their work with brain cells.

Their work suggests the brain learns not to use the eye that is deprived of sensory experience, "because the activity in that eye is not carrying any useful information," Bear says.

"Young children who have cataracts have profound visual disabilities -- a consequence of the inappropriate wiring of the visual cortex," Bear says.

From the work of Hubel and Wiesel, it has been recognized that visual problems in young children need to be corrected early. If the problem is not corrected during the first 10 years of life, when the brain is still developing, the deficit is very difficult to reverse, he adds.

Bear and his team plan to continue their work by trying to determine the special molecular features of the brain that are present during the critical period of the brain's early development when connections between the brain and the world are still being formed.

Dan Feldman, an assistant professor of biology from the University of California at San Diego, comments the experiments by Bear and colleagues "have proven, quite nicely, that sensory deprivation induces the form of synaptic weakening called LTD and that the process actually happens in the visual cortex."

"Generally, this finding helps us understand how the brain stores information about experience. And specifically, for kids who have occluded vision in one eye, we now understand why that eye's input gets disconnected from the visual cortex," Feldman says.

More information

To learn more about vision development and eye problems, visit the National Eye Institute or Prevent Blindness America.

SOURCES: Mark Bear, Ph.D., professor, neuroscience, Massachusetts Institute of Technology, Cambridge; Dan Feldman, Ph.D., assistant professor, biology, University of California, San Diego; August 2003 Nature Neuroscience
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