暴露于铝的解离小鼠海马神经元的树突运输缓慢。

Slow dendritic transport of dissociated mouse hippocampal neurons exposed to aluminum.

作者信息

Wakayama I, Song K J, Nerurkar V R, Yoshida S, Garruto R M

机构信息

Research Center of Neurological Diseases, Kansai College of Oriental Medicine, Kumatori, Osaka, Japan.

出版信息

Brain Res. 1997 Feb 14;748(1-2):237-40. doi: 10.1016/s0006-8993(96)01314-5.

DOI:10.1016/s0006-8993(96)01314-5

PMID:9067468

Abstract

We determined the influence of aluminum on dendritic transport, using an in vitro system of dissociated mouse hippocampal neurons. Newly synthesized RNA from dissociated mouse hippocampal neurons was more slowly transported into dendrites in the presence of aluminum chloride when compared to those without the addition of aluminum chloride to the culture medium. Suppression of dendritic transport of newly synthesized RNA may be responsible for the dendritic degeneration observed in aluminum neurotoxicity, eventually leading to neuronal degeneration.

摘要

我们使用解离的小鼠海马神经元体外系统，确定了铝对树突运输的影响。与培养基中未添加氯化铝的情况相比，在存在氯化铝的情况下，解离的小鼠海马神经元新合成的RNA向树突的运输更慢。新合成RNA的树突运输受抑制可能是铝神经毒性中观察到的树突退化的原因，最终导致神经元退化。