1995 Fiscal Year Final Research Report Summary
Pharmacological Analysis of Neurite Re-elongation
| Project/Area Number |
06454612
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
応用薬理学・医療系薬学
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SAITO Hiroshi Univ.of Tokyo, Fac.Pharm.Sci., Prof., 薬学部, 教授 (00012625)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIYAMA Nobuyoshi Univ.of Tokyo, Fac.Pharm.Sci., Res.Assoc., 薬学部, 助手 (20201692)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Polyamines / Spermine / Interleukin-2 / Cultured Neuron Cell / Hippocampus / Interleukin-6 / Axonal Branching / Epilepsy |
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| Research Abstract |
The object of our project was to search for substances which promote neurite re-elongation and branching in the lesioned neurons and to clarify the pharmacological mechanisms for such activity. In 1994, we demonstrated that polyamines strongly promoted neurite re-elongation. When spermine, one of the polyamines, was cotreated with basic fibroblast growth factor, which had been shown to promote neurite branching, they promoted both neurite re-elongation and branching on the same neurons. These results indicated that neurite re-clongation and branching are regulated independently. In 1995, we found that interleukin-2 (IL-2), but not IL-6, enhanced the neurite branching, although both of them had been shown to exert neurotrophic action on intact (undamaged) neurons. These results suggest that IL-2 and Il-6 has distinct effect on neuronal regeneration in central neurons. From these results, polyamines and IL-2 are now established for candidate agents for the treatment of brain lesions induced by such as stroke or cerebral ischemia. More recently, we demonstrated, utilizing hippocampal slice culture technique, that epileptiform activity produced by GABA antagonist picrotoxin prevents synapse formation of hippocampal mossy fibers via L-type calcium channel activation in physically lesioned neuronal network.
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