α-突触核蛋白原纤维诱导的帕金森病小鼠模型的行为表型及病理特征

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Abstract Objective: To study the behavioral phenotype and pathological features of A53T mutant α-synuclein (A53T αS) fibril mice model of Parkinson’s disease (PD). Methods: A53T αS fibril PD model was established by injecting 5 μg of A53T αS into the substantia nigra pars compacta (SNpc) of mice brain for 3 months. The motor and cognitive behavioral phenotypes of the model mice were studied by open field test, hanging test and Y maze. Anti-phosphorylation of α-synuclein (pSyn), anti-tyrosine hydroxylase (TH) and microglia-specific protein antibody IBA-1 were used as molecular markers of Lewy bodies (LBs), dopamine (DA) neurons and neuroinflammation, respectively. These markers were used for immunohistochemical staining to evaluate the typical pathological characteristics in the brain of PD model mice. Results: In the open field test, total locomotive distance was almost equal in both groups of mice (P>0.05); however, duration of the four-jaw grip of the model mice in the hanging test was much shorter than that of the control mice (P<0.05). In the Y maze test, the correct rate of spontaneous alterations of the model mice was a bit lower than that of the control mice, but there was no significant difference (P>0.05). Compared with the control mice, the number of pSyn-positive inclusions and IBA-1 positive cells in the SNpc region of the model mice were markedly increased (P<0.01), whereas the number of TH-positive neurons was notably decreased (P<0.05). Conclusion: Intra-nigral injection of A53T αS fibrils can stably induce a mouse model of PD, which exhibits a certain decline in motor function and can simultaneously recapitulates the typical pathological features of PD, such as LBs, the degeneration of DA neurons, and over-activated neuroinflammation as well.

Key words： Parkinson’s disease model α-synuclein fibril behavior Lewy bodies dopamine neurons mice

Received: 18 October 2018

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	TIAN Jing
	HOU Zhidong
	REN Xiangpeng.

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https://xb.wmu.edu.cn/EN/ OR https://xb.wmu.edu.cn/EN/Y2019/V49/I3/157

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