NMDA受体
谷氨酸受体
受体
内分泌学
生物
内科学
泽尔韦格综合征
癫痫
神经科学
病理生理学
过氧化物酶体
医学
作者
Pierre Gressèns,Myriam Baes,Philippe Leroux,Alain Lombet,Paul Van Veldhoven,Ann Janssen,Jòseph Vamecq,Stéphane Marret,Philippe Evrard
标识
DOI:10.1002/1531-8249(200009)48:3<336::aid-ana8>3.0.co;2-q
摘要
Disorders of neuronal migration in cerebral cortex are associated with neurological impairments, including mental retardation and epilepsy. Their causes and pathophysiology remain largely unknown, however. In patients with Zellweger disease, a lethal panperoxisomal disorder, and in mice lacking the Pxr1 import receptor for peroxisomal matrix proteins, the absence of peroxisomes leads to abnormal neuronal migration. Analysis of Pxr1-/- mice revealed that the migration defect was caused by altered N-methyl-D-aspartate (NMDA) glutamate receptor-mediated calcium mobilization. This NMDA receptor dysfunction was linked to a deficit in platelet-activating factor, a phenomenon related to peroxisome impairment. These findings confirm NMDA receptor involvement in neuronal migration and suggest a link between peroxisome metabolism and NMDA receptor efficacy.
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