Protein critical for neuromuscular junction modulates glutamate

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Protein critical for neuromuscular junction

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Lrp4 in astrocytes modulates glutamatergic transmission

Published online June 13 2016

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“We found that glutamate release in the brain was impaired in mice lacking low-density lipoprotein receptor–related protein 4 (Lrp4), a protein that is critical for neuromuscular junction formation.”

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Could this relate to POTS which improves with mestinon? or chronic fatigue of so many conditions (CRPS, fibromyalgia, Lyme Disease)?

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As reported in Neuroscience News

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“In the neuromuscular juncture, Mei’s lab found several years back that LRP4 on the muscle cell surface is a receptor for agrin, a protein that motor neurons release to direct construction of the nerve-muscle juncture. His lab later identified antibodies to LRP4 and agrin as new causes of myasthenia gravis. The new research indicates that release of ATP by astrocytes is also regulated by agrin signaling.”

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…”When you take LRP4 out of astrocytes, ATP levels released by those astrocytes go super high, which suppresses glutamate transmission,” Mei said.

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“Now it’s clear that glial cells, like astrocytes, have a role in neurodevelopment and longer-term in regulating communication between two neurons.”

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Original Research from the Medical College of Georgia: by Xiang-Dong Sun, Lei Li, Fang Liu, Zhi-Hui Huang, Jonathan C Bean, Hui-Feng Jiao, Arnab Barik, Seon-Myung Kim, Haitao Wu, Chengyong Shen, Yun Tian, Thiri W Lin, Ryan Bates, Anupama Sathyamurthy, Yong-Jun Chen, Dong-Min Yin, Lei Xiong, Hui-Ping Lin, Jin-Xia Hu, Bao-Ming Li, Tian-Ming Gao, Wen-Cheng Xiong and Lin Mei in Nature Neuroscience. 

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