Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss.

@article{Talantova2013AIA,
  title={Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss.},
  author={Maria Talantova and Sara Sanz-Blasco and Xin Zhang and Peng Xia and Mohd Waseem Akhtar and Shu-ichi Okamoto and Gustavo Dziewczapolski and Tomohiro Nakamura and Gang Cao and Alexander E. Pratt and Yeon-Joo Kang and Shichun Tu and Elena Molokanova and Scott R Mckercher and Samuel Andrew Hires and Hagit Sason and David G. Stouffer and Matthew W Buczynski and James P. Solomon and Sarah Michael and Evan T Powers and Jeffery W Kelly and Amanda Roberts and Gary Tong and Traci Fang-Newmeyer and James Parker and Emily A. Holland and Dongxian Zhang and Nobuki Nakanishi and H. V. Chen and Herman Wolosker and Yuqiang Wang and Loren Howell Parsons and Rajesh Ambasudhan and Eliezer Masliah and Stephen F. Heinemann and Juan C Pi{\~n}a-Crespo and Stuart Lipton},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2013},
  volume={110 27},
  pages={E2518-27}
}
Synaptic loss is the cardinal feature linking neuropathology to cognitive decline in Alzheimer's disease (AD). However, the mechanism of synaptic damage remains incompletely understood. Here, using FRET-based glutamate sensor imaging, we show that amyloid-β peptide (Aβ) engages α7 nicotinic acetylcholine receptors to induce release of astrocytic glutamate, which in turn activates extrasynaptic NMDA receptors (eNMDARs) on neurons. In hippocampal autapses, this eNMDAR activity is followed by… CONTINUE READING
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