LTD-inducing stimuli promote cleavage of the synaptic adhesion molecule NGL-3 through NMDA receptors, matrix metalloproteinases, and presenilin/g-secretase

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Title
LTD-inducing stimuli promote cleavage of the synaptic adhesion molecule NGL-3 through NMDA receptors, matrix metalloproteinases, and presenilin/g-secretase
Author(s)
Hyejin Lee; Eun-Jae Lee; Yoo Sung Song; Eun Joon Kim
Publication Date
2014-01
Journal
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, v.369, no.1633, pp.20130158 -
Publisher
ROYAL SOC
Abstract
Long-term depression (LTD) reduces the functional strength of excitatory synapses through mechanisms that include the removal of AMPA glutamate receptors from the postsynaptic membrane. LTD induction is also known to result in structural changes at excitatory synapses, including the shrinkage of dendritic spines. Synaptic adhesion molecules are thought to contribute to the development, function and plasticity of neuronal synapses largely through their trans-synaptic adhesions. However, little is known about how synaptic adhesion molecules are altered during LTD. We report here that NGL-3 (netrin-G ligand-3), a postsynaptic adhesion molecule that transsynaptically interacts with the LAR family of receptor tyrosine phosphatases and intracellularly with the postsynaptic scaffolding protein PSD-95, undergoes a proteolytic cleavage process. NGL-3 cleavage is induced by NMDA treatment in cultured neurons and low-frequency stimulation in brain slices and requires the activities of NMDA glutamate receptors, matrix metalloproteinases (MMPs) and presenilin/g-secretase. These results suggest that NGL-3 is a novel substrate of MMPs and g-secretase and that NGL-3 cleavage may regulate synaptic adhesion during LTD.
URI
https://pr.ibs.re.kr/handle/8788114/1156
ISSN
0962-8436
Appears in Collections:
Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > Journal Papers (저널논문)
Files in This Item:
2014-Philosophical transactions - LTD-inducing stimuli.pdfDownload

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