| Co-Investigator(Kenkyū-buntansha) |
FURUKAWA Shoei Gifu Pharmaceutical College,Molecular biology, Associate Professor, 分子生物学, 助教授 (90159129)
OYANAGI Kiyomitsu Niigata University,Brain Research Institute, Associate Professor, 脳研究所, 助教授 (00134958)
YAMADA Mitsunori Niigata University,Brain Research Institute, Research Associate, 脳研究所, 助手 (30240039)
TAKAHASHI Hitoshi Niigata University,Brain Research Institute, Associate Professor, 脳研究所, 助教授 (90206839)
武田 茂樹 新潟大学, 脳研究所, 助教授 (90134957)
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| Research Abstract |
The process of brain lesion repair is closely related to the presence of astrocytes and their activity. We can conclude that there are at least three different repair processes of brain lesions, namely, (1) the process in the well-developed brain with healthy astrocytes, (2) the process in the well-developed brain with diseased astrocytes and (3) the process in the developing brain without astrocytes.
The occurence and the degree of increased intracranial pressure (IICP) during the process of brain lesion repair are also closely related to the presence of astrocytes and their activity. In the adult brain where healthy astrocytes present, early brain swelling after injury is due to the swelling of astrocytes surrounding the diseased neurons, and the subsequent severe increase of brain volume is due to the accumulation of edema fluid in the extracellular space, causing the IICP of various degrees.
In the case of hepatocerebral degeneration, severe and diffuse brain swelling, not brain edema, occurs in the acute stage without any noticeable focal lesions. This is due to the primary swelling of the diseased astrocytes, being responsible for the IICP.
The developing fetal brain originally possess a wide extracellular space, but little or no astrocytes. Therefore, the swelling of astrocyte or the accumulation of edema fluid in the extracellular space is not the feature in the diseased fetal brain. The IICP does not take place.
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