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UC Berkeley neuroscientist receives 2001 Ameritec Prize for research that could help cure paralysis
09 November 2001

By Robert Sanders, Media Relations

 

Mu-ming Poo

University of California, Berkeley, neuroscientist Mu-ming Poo.


Berkeley - University of California, Berkeley, neuroscientist Mu-ming Poo will receive the 2001 Ameritec Prize tomorrow (Sat., Nov. 10) for research that could pave the way for an eventual cure for paralysis.

Poo, a professor of molecular and cell biology at UC Berkeley and a member of the Wills Neuroscience Institute, will share the award with Marie T. Filbin of Hunter College, City University of New York.

The $40,000 prize will be presented to the scientists at the Neurotrauma Symposium in San Diego, part of the annual Society for Neuroscience meeting.

Filbin and Poo share the eighth Ameritec Prize, established in 1987 to recognize scientists whose research advances the search towards a cure for paralysis. Winners of the prize, funded by the nonprofit Ameritec Foundation of Covino, Calif., are chosen by an advisory board of prominent medical researchers.

Poo, who came to UC Berkeley from UC San Diego last year as the Class of 1933 Professor of Neurobiology, studies the way the nervous system organizes itself in the developing organism. Of particular interest is the way nerve cells find the right connections and set up contacts, or synapses, with other nerve cells so that they can talk to one another, and how these connections are modified as the organism learns.

To get answers to these questions, he takes advantage of the easily accessible nerve cells of the aquatic frog Xenopus laevis.

He and his colleagues found, for example, that while the growing tips of nerve cells sniff their way along trails of "guidance" chemicals in the nervous system, altering levels of a signaling molecule inside the nerve cell can change the way the nerve cell responds to these chemicals. Instead of growing towards these chemical guidance cues, the cell steers away from them. This change in behavior comes about by knocking down levels of cyclic AMP or cyclic GMP, cyclic nucleotides common to many cells.

Conversely, they showed that the repulsive response induced by other guidance cues can be converted into attraction by increasing the level of cyclic nucleotides.

"One of my contributions to the basic field of developmental neurobiology is to say that it's not correct to talk about a guidance molecule as 'chemoattractant' or 'chemorepellent,'" Poo said. "Each factor can be an attractant or a repellent, depending on conditions in the cell. These conditions are set by many other factors the cell responds to, such as hormones in the extracellular environment. The cyclic nucleotide level represents an integration of all these coincident signals and determines how the cell responds to the guidance factors."

This finding has great potential in treating humans who have sustained spinal cord injuries, Poo said.

"For a potential cure for paralysis, one needs to overcome the inhibitory factors in regenerating nerve cells after injury," he said. "Using drugs to alter cyclic nucleotide levels and change an inhibition into an attraction offers the potential to overcome that."

Filbin, a native of Northern Ireland, has already shown in rats that drugs that increase cyclic AMP levels in nerve cells can make the cells ignore "inhibitors" and regrow into damaged areas, thus promoting nerve regeneration after injury.

Poo, 53, was born in Nanjing, China, and received his PhD from Johns Hopkins University in 1974. He held faculty positions at UC Irvine, Yale University School of Medicine, Columbia University and UC San Diego before coming to UC Berkeley a year ago.

He is a member of UC Berkeley's Health Sciences Initiative, a broad campus effort to tackle major problems affecting the health of people worldwide.

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