Transient receptor potential V1 modulates neuroinflammation in Parkinson’s disease dementia: Molecular implications for electroacupuncture and rivastigmine

Document Type : Original Article

Authors

1 Department of Neurology, China Medical University Hospital, Taichung, Taiwan

2 Graduate Institute of Acupuncture Science, College of Chinese Medicine, China Medical University, Taichung, Taiwan

3 Everflourish Neuroscience and Brain Disease Center, China Medical University Hospital, Taichung, Taiwan

4 Department of Chinese Medicine, China Medical University Hospital, Taichung, Taiwan

5 College of Medicine, China Medical University, Taichung, Taiwan

6 Department of Psychiatry, Taoyuan Psychiatric Center, Ministry of Health and Welfare, Taoyuan, Taiwan

7 Chinese Medicine Research Center, China Medical University, Taichung, Taiwan

Abstract

Objective(s): Parkinson’s disease (PD) is a common progressive neurodegeneration disease. Its incidence increases with age and affects about 1% of people over 60. Incidentally, transient receptor potential V1 (TRPV1) and its relation with neuroinflammation in mouse brain has been widely reported.
Materials and Methods: We used 6-hydroxydopamine (6-OHDA) to induce PDD in mice. We then used the Morris water maze and Bio-Plex to test learning and inflammatory mediators in mouse plasma. Western blotting and immunostaining were used to examine TRPV1 pathway in the hippocampus and medial prefrontal cortex (mPFC).
Results: On acquisition days 3 (Control = 4.40 ± 0.8 sec, PDD = 9.82 ± 1.52 sec, EA = 5.04 ± 0.58 sec, Riva = 4.75 ± 0.87 sec; P=0.001) and 4, reversal learning days 1, 2, 3 (Control = 2.86 ± 0.46 sec, PDD = 9.80 ± 1.83 sec, EA = 4.6 ± 0.82 sec, Riva = 4.6 ± 1.03 sec; P=0.001) and 4, PDD mice showed significantly longer escape latency than the other three groups. Results showed that several cytokines were up-regulated in PDD mice and reversed by EA and rivastigmine. TRPV1 and downstream molecules were up-regulated in PDD mice and further reversed by EA and rivastigmine. Interestingly, α7 nicotinic receptors and parvalbumin levels in both the hippocampus and prefrontal cortex increased in EA-treated mice, but not in rivastigmine-treated mice.
Conclusion: Our results showed that TRPV1 played a role in the modulation of neuroinflammation of PDD, and could potentially be a new target for treatment.

Keywords


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