Douhou Aïcha, Debeir Thomas, Murer Mario Gustavo, Do Louis, Dufour Noëlle, Blanchard Véronique, Moussaoui Saliha, Bohme Georg Andrees, Agid Yves, Raisman-Vozari Rita
INSERM U-289, Hôpital de la Salpétriêre, Paris, France.
Exp Neurol. 2002 Jul;176(1):247-53. doi: 10.1006/exnr.2002.7935.
The effects of a chronic treatment with the anti-glutamate and sodium channel modulating neuroprotective agent riluzole on the degeneration of dopamine-containing neurons were studied in the brain of weaver mutant mice. In these animals, as in Parkinson's disease, dopaminergic neurons of the nigro-striatal pathway undergo spontaneous and progressive cell death. Homozygous weaver mice were orally treated twice a day with either 8 mg/kg riluzole or placebo for 2 months. Quantification of tyrosine-hydroxylase and dopamine-transporter axonal immunostaining in the striatum revealed that riluzole significantly increased the density of striatal dopaminergic nerve terminals. These results suggest that riluzole protects dopaminergic processes in the weaver mice and/or promotes their neuroplasticity.
在织工突变小鼠的大脑中,研究了抗谷氨酸和钠通道调节神经保护剂利鲁唑长期治疗对含多巴胺神经元变性的影响。在这些动物中,如同在帕金森病中一样,黑质-纹状体通路的多巴胺能神经元会发生自发性和进行性细胞死亡。纯合子织工小鼠每天口服两次8mg/kg利鲁唑或安慰剂,持续2个月。对纹状体中酪氨酸羟化酶和多巴胺转运体轴突免疫染色进行定量分析,结果显示利鲁唑显著增加了纹状体多巴胺能神经末梢的密度。这些结果表明,利鲁唑可保护织工小鼠的多巴胺能神经元过程和/或促进其神经可塑性。