1996 Fiscal Year Final Research Report Summary
Mechanism of Ischemic Neuronal Death : Neuron, Glial interaction
| Project/Area Number |
07670692
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Tohoku University |
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Principal Investigator |
NAKAMURA Shozo Tohoku Univ. Hospital lecturer, 医学部・附属病院, 講師 (80108498)
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| Co-Investigator(Kenkyū-buntansha) |
TAKEDA Atsushi Tohoku Univ. School of Medicine Assistant Prof, 医学部, 助手 (70261534)
ITOYAMA Yasuto Tohoku Univ. School of Medicine Professor, 医学部, 教授 (30136428)
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| Project Period (FY) |
1995 – 1996
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| Keywords | ischemia / cytokine / oxidative stress / antioxidant / neurotrophic factor / inflammation / neuronal death |
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| Research Abstract |
The present was designed to study (1) glial cell activation, and (2) heparin-binding growth-associated molecule exression after ischemia in order to obtain a clue to prevent ischemia-induced dementia.
(1) Induction of stress-activated molecules in the glial cells
Microglial cells were activated after ischemia and presented various immuno-reactive molecules. Astroglial cells presented stress proteins, such as HSP27. Neutrophils in ischemic areas expressed cell adhesion molecules. These data suggest that chemicals that can intervene immunological processes could be promissing for the treatment of ischemic brain injury.
(2) Neurotrophic substances and ischemia
We focused upon heparin-binding growth-associated molecules (HB-GAM), as HB-GAM shows trophic effects on various types of neurons. We observed that HB-GAM is expressesd in normal CA1 pyramidal neurons. After ischemic death of CA1 neuron, HB-GAM expression in the CA1 subfield was markedly enhanced and reactive astrocytes were the major source of HB-GAM.The level of Syndecan-3, the receptor for HB-GAM,was also altered after ischemia. These results suggest that HB-GAM may play an important role for neuronal survival and synaptic rearrangement.
Bifemelane hydrochloride (BF) is a modulator of cholinergic systems and increases muscarinic cholinergic receptor density. Animals treated with BF for one-hundred days after ischemia showed increased cholinesterase activity in the hippocampus. Thus, modulation of cholinergic system could be beneficial for the treatment of post-ischemic brain dysfunction.
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