Funded by almost $350,000 in grants from the National Institutes of Health and the American Heart Association, Yang Li, Ph.D., assistant professor of neuroscience, and Christian Stork, a doctoral student in molecular and cellular biology, are indeed breaking new ground in understanding the role of zinc in ischemic stroke.

Their paper, “Intracellular Zinc Elevation Measured with a ‘Calcium-Specific’ Indicator during Ischemia and Reperfusion in Rat Hippocampus: A Question on Calcium Overload,” published in The Journal of Neuroscience,* revealed research that showed the importance of an “overload” of intracellular zinc as opposed to that of calcium, which previously had been suspected as the primary culprit facilitating ischemic neuronal cell death.

Fluorescent imaging of zinc and calcium ions in acute rat hippocampal slices during ischemia (simulated by oxygen and glucose deprivation) led to their findings.

The question of the role of zinc and calcium ions in ischemic stroke was first explored by Li and Stork in 2005.

Following a stroke, if the brain is deprived of oxygen because of a blood clot, tissues or neurons accumulate a large amount of calcium. But calcium isn't’t the only substance rising in the brain after a stroke, says Li. Li and Stork found zinc would do the same. Although the preponderance of treatments and clinical trials had targeted calcium, Li noted that they had not been successful in affecting ischemic stroke. Li and Stork’s work led to the development of a zinc model, which departed from traditional calcium ones.

“Zinc ‘cross talks’ with other proteins in neurons in ischemic condition,” says Li.

The next step in their research is to further investigate the cellular and molecular role of zinc during ischemic stroke and take a closer look at interactions of zinc and calcium ions. Ohio University’s Perspectives magazine featured Li and Stork’s work in its autumn-winter 2006 issue.

*(Oct. 11, 2006, 26(41):10430-10437; doi:10.1523/JNEUROSCI.1588-06.2006)