Lowly cytokine may play role in controlling neurotr...( ase. We won...)

"We wondered that since there was glutamate and TNF-alpha present in the spinal cord after injury, then maybe TNF-alpha is actually enhancing the killing effect of the normal neurotransmitter," Beattie said.

In testing this, they exposed nerve cells first to glutamate and then to TNF-alpha. Separately, neither had an impact on the normal killing effect. But when they exposed the cells to even small amounts of both compounds, the killing effect increased 120 percent.

"This was a complete surprise and validated our hypothesis," Bresnahan said.

The real question, however, was in the details of the process - how exactly was the killing effect enhanced. For help with the answer, they turned to Beattie's brother Eric, a post-doctoral researcher at Stanford. The lab in which Eric Beattie was conducting research was looking at the role glutamate played in signal transmission in learning and memory.

"We wanted to know if TNF-alpha was regulating the number of receptors on the cell surface," Bresnahan explained. "If the number of receptors increased, and if there was glutamate nearby to bind to them, that would allow more calcium into the cells, killing them."

Experiments at the Stanford lab were able to show that controlling the presence or activity of TNF-alpha had a direct relationship to the numbers of glutamate receptors on the cell surface and
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Contact: Michael Beattie
beattie.2@osu.edu
614-688-8327
Ohio State University
22-Mar-2002