2022 Fiscal Year Final Research Report
Does the combination of nicotine and ethanol facilitate or block dopaminergic neuron damage in Parkinson's disease models?
| Project/Area Number |
19K10687
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 58040:Forensics medicine-related
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| Research Institution | Kagawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
塚本 郁子 香川大学, 医学部, 寄附講座教員 (10183477)
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| Project Period (FY) |
2019-04-01 – 2023-03-31
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| Keywords | Ethanol / nicotine / dopamine |
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| Outline of Final Research Achievements |
EtOH (2.0 and 3.0 g/kg) alone reversed the effects of MPTP treatment in both studied brain regions, as evidenced by an increase in DA, DOPAC, and HVA levels, TH expression, and Ser31 phosphorylation compared to the control, indicating restorative effects on striatal and hippocampal DA neurons in the MPTP model. Likewise, NIC (1.0 and 2.0 mg/kg) alone reversed MPTP treatment effects, with treated mice showing increased DA, DOPAC, and HVA contents, TH expression, and Ser31 phosphorylation compared to control mice. Co-administration of EtOH (2.0 g/kg) and NIC (1.0 mg/kg) further increased DA and HVA tissue contents, TH expression, and Ser31 phosphorylation, indicating an additive effect.
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| Free Research Field |
Neuroscience
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| Academic Significance and Societal Importance of the Research Achievements |
Our results show that EtOH and NIC induce similar increases in brain DA and TH via TH phosphorylation activation in MPTP model mice. EtOH and NIC showed an additive effect in combination, suggesting that their co-application could be a potent therapeutic strategy for treating PD.
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