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偏侧帕金森病小鼠模型中的单侧嗅觉缺陷

Unilateral olfactory deficit in a hemiparkinson's disease mouse model.

作者信息

Valle-Leija Pablo, Drucker-Colín René

机构信息

Department of Molecular Neuropathology, Institute of Cellular Physiology, National Autonomous University of Mexico, Mexico D.F., Mexico.

出版信息

Neuroreport. 2014 Aug 20;25(12):948-53. doi: 10.1097/WNR.0000000000000218.

Abstract

Parkinson's disease is a neurodegenerative disease which often presents hyposmia (80-90% of the cases). We characterized the olfactory behavior in the model of 6-hydroxydopamine of Parkinson's disease. Mice were trained to discriminate between two odorants in a radial maze. One of the odorants was associated with water as a reward. 6-hydroxydopamine was injected directly into the dorsal striatum; after complete striatal denervation, olfactory performance was evaluated in a radial maze. In the first evaluation, experimental mice performed as control mice. After the first evaluation, the narine of the contralateral side to the striatal injection was closed and mice were evaluated again. The experimental group completely lost the capacity to discriminate between the odorant associated with the reward (heptaldehyde) and the unconditioned odorant (2-heptanone). We propose that the olfactory deficit was caused by dopaminergic denervation to the olfactory tubercle and nucleus accumbens.

摘要

帕金森病是一种神经退行性疾病,常伴有嗅觉减退(80%-90%的病例)。我们对帕金森病6-羟基多巴胺模型中的嗅觉行为进行了特征描述。小鼠在放射状迷宫中接受训练,以区分两种气味剂。其中一种气味剂与作为奖励的水相关联。将6-羟基多巴胺直接注射到背侧纹状体;在完全纹状体去神经支配后,在放射状迷宫中评估嗅觉表现。在第一次评估中,实验小鼠的表现与对照小鼠相同。在第一次评估后,封闭纹状体注射对侧的鼻孔,再次对小鼠进行评估。实验组完全丧失了区分与奖励相关的气味剂(庚醛)和无条件气味剂(2-庚酮)的能力。我们认为嗅觉缺陷是由嗅觉结节和伏隔核的多巴胺能去神经支配引起的。

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