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Nerve navigation findings prompt new direction for spinal cord research

A piece of the puzzle of how nerves find their way across the midline of the brain and spinal cord in a developing embryo has been found by Medical College of Georgia researchers.

They have found that an enzyme called focal adhesion kinase tells the arm-like extension of a neuron to cross the midline of the spinal cord, says Dr. Wen-Cheng Xiong, developmental neurobiologist and lead author on the paper in the November issue of Nature Neuroscience.

After crossing, the axon becomes part of the complex network that enables the right side of the brain to control the left side of the body and vice versa.

The finding helps explain normal development of the nervous systems and provides a new target in the search for ways to re-establish connections and the movement and feeling they enable lost to spinal cord injuries.

"This kinase plays a role in helping direct axon movement across the spinal cord during development," Dr. Xiong says. "How it does that is one of the questions we hope to answer next. We still have a lot of questions." Among those is why this mechanism doesn't seem to work after development is complete. "If the spinal cord is injured, why doesn't it re-cross that boundary?" she says. "Why are these molecules not functioning well in the adult?"

Focal adhesion kinase already is a hot topic among scientists studying how cells migrate and how tumor cells spread. Now, Dr. Xiong and her collaborators have found the enzyme also plays an important role in central nervous system development.

She explains that for axons to journey across the spinal cord, floor plate cells along this natural midline of the developing body secrete a guidance or cue factor called netrin-1. "If this molecule is deleted, this axon cannot cross. It just stays on this side" and the developing embryo will die, a testimony to netrin's expansive role in getting cells where they need to be. "T
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Contact: Toni Baker
tbaker@mcg.edu
706-721-4421
Medical College of Georgia
26-Oct-2004


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