2014.02.12 Press Release

Towards unraveling the cell death mechanism in brain ischemia

The National Institute for Physiological Sciences and Associate Professor Ko Matsui's group at the Tohoku University School of Medicine has discovered a new role of glial cells in the brain by using new technology that allows optical control over cell activity.

The following four major points were discovered in this research:

1. Glutamate, a neurotransmitter, is released from the glial cells which can affect brain functions such as learning and memory.

2. When the activity of glial cells becomes abnormal, excess glial release of glutamate occurs which causes brain cell death.

It was previously known that during brain ischemia, acidosis of brain tissue occurs along with excess releases of glutamate; however, the cellular source of glutamate was unclear.

3. A new mechanism was discovered where the acidosis of the cytoplasm of the glial cells was the direct trigger of glutamate release from glial cells.

4. This research further established, by alkalizing the glial cells through optical control technology, the release of glutamate was inhibited which led to the slowing of brain cell death progression during ischemia.

These findings are expected to lead to new medical treatments of strokes.

The results of the research have been published in Neuron on January 22, 2014 (January 23 JST). The paper's title is "Optogenetic Countering of Glial Acidosis Suppresses Glial Glutamate Release and Ischemic Brain Damage."

This research was conducted through grants from the Ministry of Education, Culture, Sports, Science & Technology Grant-in-Aid for Scientific Research and the Takeda Science Foundation.

Associate Professor Ko Matsui
Division of Interdisciplinary Medical Science, Center for Neuroscience,
Tohoku University Graduate School of Medicine
TEL: +81-22-717-8208
FAX: +81-22-717-8594
E-mail: matsui* (Replace * with @)

[Public Relations]
Lecturer Hitoshi Inada
Public Relations Office of Tohoku University Graduate School of Medicine
TEL: +81-22-717-7891
FAX: +81-22-717-8187
E-mail: hinada* (Replace * with @)