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Park, Chan Young
Calcium Dynamics Lab
Research Interests
  • Calcium Signaling, calcium Channels, immune, neuroscience, drug Development

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Gabapentin Receptor alpha 2 delta-1 Is a Neuronal Thrombospondin Receptor Responsible for Excitatory CNS Synaptogenesis

Cited 216 times inthomson ciCited 206 times inthomson ci
Title
Gabapentin Receptor alpha 2 delta-1 Is a Neuronal Thrombospondin Receptor Responsible for Excitatory CNS Synaptogenesis
Author
Eroglu, CaglaAllen, Nicola J.Susman, Michael W.O'Rourke, Nancy A.Park, Chan YoungOezkan, EnginChakraborty, ChandraniMulinyawe, Sara B.Annis, Douglas S.Huberman, Andrew D.Green, Eric M.Lawler, JackDolmetsch, RicardoGarcia, K. ChristopherSmith, Stephen J.Luo, Z. DavidRosenthal, ArnonMosher, Deane F.Barres, Ben A.
Issue Date
2009-10
Publisher
CELL PRESS
Citation
CELL, v.139, no.2, pp.380 - 392
Abstract
Synapses are asymmetric cellular adhesions that are critical for nervous system development and function, but the mechanisms that induce their formation are not well understood. We have previously identified thrombospondin as an astrocyte-secreted protein that promotes central nervous system (CNS) synaptogenesis. Here, we identify the neuronal thrombospondin receptor involved in CNS synapse formation as α2δ-1, the receptor for the anti-epileptic and analgesic drug gabapentin. We show that the VWF-A domain of α2δ-1 interacts with the epidermal growth factor-like repeats common to all thrombospondins. α2δ-1 overexpression increases synaptogenesis in vitro and in vivo and is required postsynaptically for thrombospondin- and astrocyte-induced synapse formation in vitro. Gabapentin antagonizes thrombospondin binding to α2δ-1 and powerfully inhibits excitatory synapse formation in vitro and in vivo. These findings identify α2δ-1 as a receptor involved in excitatory synapse formation and suggest that gabapentin may function therapeutically by blocking new synapse formation.
URI
https://scholarworks.unist.ac.kr/handle/201301/7170
URL
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=70350368006
DOI
10.1016/j.cell.2009.09.025
ISSN
0092-8674
Appears in Collections:
BME_Journal Papers
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