Vladimir Parpura, Zoology and Genetics, (515) 294-8206
Teddi Barron, News Service, (515) 294-4778


AMES, Iowa -- Research conducted at Iowa State University could change our understanding of how the brain works and lead to new avenues of treatment for stroke, epilepsy and head injury.

Results of a two-year study by Iowa State neuroscientists Vladimir Parpura and Philip Haydon will appear in today's (July 18) issue of "Proceedings of the National Academy of Sciences." The paper, "Physiological Astrocytic Calcium Levels Stimulate Glutamate Release to Modulate Adjacent Neurons," gives evidence supporting a relatively new theory about communications between brain cells.

The brain has two types of cells--neurons and glia. Neurons contain neurotransmitters, which are chemicals that trigger signals to pass messages. Until recently, neuroscientists believed neurons were the only brain cells transmitting message signals. Glial cells were thought to serve only as support.

In the mid-1990s, however, Parpura and Haydon were among the first researchers to discover that glial cells are much more important to the brain's communication network than previously thought. Their 1994 paper, published in "Nature," showed that a type of glial cell—the astrocyte—releases glutamate (a neurotransmitter) and signals neurons.

"This release of glutamate is controlled by increased levels of calcium in the astrocytes. Exactly how much calcium was needed to cause the glutamate release was unclear. We didn't know if it was in the normal range for calcium levels in astrocytes. That's the question we answered in the current study," Parpura said.

Parpura and Haydon found the amount of calcium to be within the normal range, indicating that astrocytes are part of the brain's communication network.

The findings may also open new possibilities for treatment of illnesses such as stroke, epilepsy and head injury where glutamate toxicity is known to contribute to brain tissue damage, Parpura said.

"While our findings implicate astrocytes as the additional site for glutamate release under normal conditions, it is tempting to speculate that high calcium levels in astrocytes could cause excess release of glutamate, and play a role in disease," he said.

"This sheds new light on where to look for treatment. There's potential for developing new drugs that could interfere with the release of glutamate," he said.

While the research is still in its early states, Parpura said the ramifications could be great. "Neurons make up only 10 percent of the brain's cells, yet that's what we've always focused on. There's 90 percent of the brain yet to learn about. It's uncharted area," Parpura said.

Copies of the paper are available from the "Proceedings of the National Academy of Sciences" news office,
(202) 334-2138, E-mail pnasnews@nas.org.


Note to editors: The news office of "Proceedings of the National Academy of Sciences" distributed the following summary of the Iowa State research in a news release.

The two major types of brain cells, neurons and glia, have long been thought to play distinct roles in the central nervous system. While neurons have been viewed as signal transmitters, glia have been pegged as providers of structural support. The results of several recent studies, however, suggest that glia also may be actively involved in neural signaling. Specifically, researchers have shown that signaling activity among neurons can increase calcium levels inside astrocytes, a subtype of glial cell. These intracellular calcium increases stimulate astrocytes to release the neurotransmitter, glutamate, which in turn signal adjacent neurons.

Whether the chain of events surrounding astrocytic glutamate release represents a normal signaling mechanism in the functional central nervous system or operates only under abnormal or pathophysiological conditions is unknown. Until now, no one has determined if levels of calcium necessary to stimulate glutamate release from astrocytes are in the normal physiological range for these cells. Researchers from Iowa State University demonstrate that intracellular calcium levels necessary to trigger glutamate release and subsequent neuron excitation are well within the range normally found in astrocytes in the body. These findings suggest that this recently identified signaling pathway involving astrocytes may modulate intercellular communication in the brain under normal conditions and even play a role in information processing. This work was supported by the Whitehall Foundation and the National Institutes of Health.

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