1992 Fiscal Year Final Research Report Summary
The research for the mechanism of ischemic cell damage in the striatum and the restoration of the neuronal basic circuit by neural transplantation
| Project/Area Number |
03454352
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Cerebral neurosurgery
|
|---|
| Research Institution | Nagoya City University Medical School |
|---|
Principal Investigator |
NAGAI Hajime Nagoya City University Medical School, Neurosurgery, Professor, 医学部, 教授 (00023747)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NISHINO Hitoo Nagoya City University Medical School, Physiology, Professor, 医学部, 教授 (60073730)
MABE Hideo Nagoya City University Medical School, Neurosurgery, Assistant Professor, 医学部, 助教授 (20093073)
|
|---|
| Project Period (FY) |
1991 – 1992
|
| Keywords | Ischema / Striatum / Transplantaion / 移植 / 学習能 / 神経伝達物質 |
|---|
| Research Abstract |
(1) An increase of extracellular release of striatal dopamine and glutamate was observed during total and focal cerebral ischemia. A D1 receptor antagonist and destruction of substantial nigra which caused decrease of striatal dopamine release prevented ischemic cell damage in the striatum. These results suggest that extracellular dopamine release in the striatum during ischemia may contribute to ischemic cell damage. A Phospholipase C inhibitor which decreased the release of arachidonic acid in the early period of ischemia decreased extracellular glutamate release in the striatum. These results suggest that the release of arachidonic acid may cause further release of glutamate in the striatum in the early period of ischemia.
(2) We implanted cell suspensions of fetal striatum into ischemic region caused by intraluminal occlusion of middle cerebral artery in the rat, and investigated survival/development of grafted cells and functional recovery. Transplantation reversed the ischemia induced behavioral deficits in the passive avoidance task and water-maze test. Dendritic outgrowth marked with Dil(1,1'-dioctadecyl-3,3,3-',3-'tetramethylindo-carbocyanine perchlorate) could be seen under fluorescent microscopy. Immunohistochemical study revealed that many ChAT(choline acetyltransferase) positive cells and GABA positive cells survived. GABA level in the globus pallidus was decreased 1 month after ischemia. Transplantation normalized the GABA level in the globus pallidus. Autoradiography revealed that muscarinc, D1, D2 and GABA receptors were developed in the grafts. Data suggest that fetal striatal cell grafting remodels the ischemic brain and ameliorates damaged functions. However, anatomical and physiological connections between the grafts and hosts could not be observed in this study. Therefore, further investigations are needed.
|
-
-
-
-
-
-
-
-
-
[Publications] Nishino, H., Koide, K., Aihara, N., Kumazaki, M., Sakurai, T., and Nagai, H.: "Striatal grafts in the ischemic striatum improve pallidal GABA release and passive avoidance." Brain Res. Bull.(1993)
Description
「研究成果報告書概要(欧文)」より
-
[Publications] Nishino, H., Aihara, N., Czurko, A., Hashitanio T., Isobe, Y., Ichikawa, O. and Watari, H.: "Reconstruction of GABAergic transmission and behavior by striatal cell grafts in rats with ischemic infarcts in the middle cerebral artery" J. Neural Transp. Plast.(1993)
Description
「研究成果報告書概要(欧文)」より
