1996 Fiscal Year Final Research Report Summary
Role of nitric oxide and glutamate in methamphetamine-induced psychosis
| Project/Area Number |
07457206
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Hokkaido University |
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Principal Investigator |
KOYAMA Tsukasa Hokkaido Univ.Medicine, Professor, 医学部, 教授 (10113557)
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| Co-Investigator(Kenkyū-buntansha) |
ODAGAKI Yuji Hokkaido Univ.Medicine, Medical Hospital, Lecturer, 医学部付属病院, 講師 (10221160)
OHMORI Tetsuro Hokkaido Univ.Medicine, Associate Professor, 医学部, 助教授 (00221135)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Schizophrenia / Methamphetamine / Nitric oxide (NO) / Dopamine |
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| Research Abstract |
Repeated abuse of methamphetamine (MA) results in schizophrenia-like psychosis in human, and this abuse produces behavioral sensitization and neurotoxicity in animals. Understanding of neuropharmacology of MA may provide insight into the pathogenesis of both MA-induced psychosis and schizophrenia. This research examined a role of nitric oxide (NO) synthesis in behavioral sensitization to MA and MA-induced neurotoxicity.
1) NO synthase inhibitor reduced the behavioral changes induced by a single administration of MA.
2) NO synthase ingibitor had no effect on MA-induced DA release in the striatum.
3) NO synthase inhibitor reduced the degree of the sensitization to MA-induced stereotypy.
4) NO synthase inhibitor attenuated the MA-induced dopaminergic neurotoxicity in the striatum.
Taken together, these results suggest that NO synthesis play a role in MA-induced acute behavioral changes and the development of behavioral sensitization to MA.Furthermore, NO synthesis has been suggested to be related to MA-induced neurotoxicity.
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