1996 Fiscal Year Final Research Report Summary
STUDY OF A NEURON-SPECIFIC PROTEIN,HPC-1, WHICH REGULATES NEURONAL SPROUTING.
Project/Area Number |
07458214
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neuroscience in general
|
Research Institution | KYORIN UNIVERSITY |
Principal Investigator |
AKAGAWA Kimio KYORIN UNIVERSITY,SCHOOL OF MEDICINE,PROFESSOR, 医学部, 教授 (80129303)
|
Co-Investigator(Kenkyū-buntansha) |
OSANAI Makoto KYORIN UNIVERSITY,SCHOOL OF MEDICINE,INSTRUCTOR, 医学部, 助手 (90286419)
FUJIWARA Tomonori KYORIN UNIVERSITY,SCHOOL OF MEDICINE,INSTRUCTOR, 医学部, 助手 (90255399)
FUJINO Ichiro KYORIN UNIVERSITY,SCHOOL OF MEDICINE,INSTRUCTOR, 医学部, 助手 (30265764)
YAMAGUCHI Kazuhiko KYORIN UNIVERSITY,SCHOOL OF MEDICINE,ASSOCIATE PROFESSOR, 医学部, 助教授 (00191221)
|
Project Period (FY) |
1995 – 1996
|
Keywords | HPC-1 / SYNTAXIN 1A / EXOCYTOSIS / NEURITE SPROUTING / REGULATED SECRETION |
Research Abstract |
This research project was carried out in order to study the physiological role of HPC-1/Syntaxin 1A.Administration of the antibody against HPC-1 resulted in increase of catechoilamine release from PC12 cells and transmitter release from autosynapse of cultured hippocampal neurons. Overexpression of HPC-1 in beta TC cell line caused decrease of insulin secretion. These results suggested that HPC-1 playd important role in regulated secratory process as a negative regulator. In dorsal root ganglion cells and cerebellar granular cells in vitro, administration of the antisense oligonucleotide against HPC-1 mRNA enhanced neurite sprouting within 12 hours. Transfection experiments with a vector carrying the antisense RNA to PC12 cells showed that suppression of HPC-1 expression caused increase of catecholamin release and enhancement of small process formation, clearly indicating the multifunctional role of HPC-1. Expression of HPC-1 gene in hippocampal neurons was suppressed by kainic acid.
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Research Products
(11 results)