Intranasal Administration of Rotenone to Mice Induces Dopaminergic Neurite Degeneration of Dopaminergic Neurons in the Substantia Nigra.
著者
笹島, 仁
(Sasajima, Hitoshi)
宮園, 貞治
(Miyazono, Sadaharu)
野口, 智弘
(Noguchi, Tomohiro)
柏柳, 誠
(Kashiwayanagi, Makoto)
上位タイトル
Biological and Pharmaceutical Bulletin
Vol.40,
No.1
(2017.
1)
,p.108-
112
識別番号
ISSN
0918-6158
DOI
10.1248/bpb.b16-00654.
その他
PMID:28049942
抄録
Exposure to environmental neurotoxins is suspected to be a risk factor for sporadic progressive neurodegenerative diseases. Parkinson's disease has been associated with exposure to the pesticide rotenone, a mitochondrial respiration inhibitor. We previously reported that intranasal administration of rotenone in mice induced dopaminergic (DA) neurodegeneration in the olfactory bulb (OB) and reduced olfactory functions. In the present study, we investigated the DA neurons in the brains of mice that were administered rotenone intranasally for an extended period. We found that the olfactory function of mice was attenuated by rotenone administration. Electrophysiological analysis of the mitral cells, which are output neurons in the OB, revealed that the inhibitory input into the mitral cells was retarded. In the immunohistochemical analysis, neurite degeneration of DA neurons in the substantia nigra was observed in rotenone-administered mice, indicating that rotenone progressively initiated the degeneration of cerebral DA neurons via the nasal route.