부산대학교 도서관

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.neuron.2006.10.035 Byline: Helen Hsieh (1)(2), Jannic Boehm (1), Chihiro Sato (3), Takeshi Iwatsubo (3), Taisuke Tomita (3), Sangram Sisodia (4), Roberto Malinow (1)(2) Keywords: MOLNEURO; SYSBIO; HUMDISEASE Abstract: Beta amyloid (A[beta]), a peptide generated from the amyloid precursor protein (APP) by neurons, is widely believed to underlie the pathophysiology of Alzheimer's disease. Recent studies indicate that this peptide can drive loss of surface AMPA and NMDA type glutamate receptors. We now show that A[beta] employs signaling pathways of long-term depression (LTD) to drive endocytosis of synaptic AMPA receptors. Synaptic removal of AMPA receptors is necessary and sufficient to produce loss of dendritic spines and synaptic NMDA responses. Our studies indicate the central role played by AMPA receptor trafficking in A[beta]-induced modification of synaptic structure and function. Author Affiliation: (1) Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 (2) Department of Neurobiology and Behavior Graduate Program, State University of New York at Stony Brook, Stony Brook, New York 11794 (3) Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan (4) Center for Molecular Neurobiology, Department of Neurobiology, Pharmacology, and Physiology, The University of Chicago, Chicago, Illinois 60637 Article History: Received 21 November 2005; Revised 10 June 2006; Accepted 26 October 2006 Article Note: (miscellaneous) Published: December 6, 2006