Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

Impaired NMDA receptor-mediated postsynaptic function and blunted NMDA receptor-dependent persistent pain in mice lacking postsynaptic density-93 protein

Academic Article
uri icon
  • Overview
  • Research
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Tao, Y. X.
  • Rumbaugh, Gavin
  • Wang, G. D.
  • Petralia, R. S.
  • Zhao, C. S.
  • Kauer, F. W.
  • Tao, F.
  • Zhuo, M.
  • Wenthold, R. J.
  • Raja, S. N.
  • Huganir, R. L.
  • Bredt, D. S.
  • Johns, R. A.

publication date

  • July 2003

journal

  • Journal of Neuroscience  Journal

abstract

  • Modification of synaptic NMDA receptor (NMDAR) expression influences NMDAR-mediated synaptic function and associated persistent pain. NMDARs directly bind to a family of membrane-associated guanylate kinases (MAGUKs) that regulate surface and synaptic NMDAR trafficking in the CNS. We report here that postsynaptic density-93 protein (PSD-93), a postsynaptic neuronal MAGUK, is expressed abundantly in spinal dorsal horn and forebrain, where it colocalizes and interacts with NMDAR subunits NR2A and NR2B. Targeted disruption of the PSD-93 gene reduces not only surface NR2A and NR2B expression but also NMDAR-mediated excitatory postsynaptic currents and potentials, without affecting surface AMPA receptor expression or its synaptic function, in the regions mentioned above. Furthermore, mice lacking PSD-93 exhibit blunted NMDAR-dependent persistent pain induced by peripheral nerve injury or injection of Complete Freund's Adjuvant, although they display intact nociceptive responsiveness to acute pain. PSD-93 appears to be important for NMDAR synaptic targeting and function and to be a potential biochemical target for the treatment of persistent pain.

subject areas

  • Animals
  • Behavior, Animal
  • Cells, Cultured
  • Excitatory Postsynaptic Potentials
  • Female
  • Freund's Adjuvant
  • Guanylate Kinase
  • In Vitro Techniques
  • Intracellular Signaling Peptides and Proteins
  • Male
  • Membrane Proteins
  • Mice
  • Mice, Knockout
  • Nerve Tissue Proteins
  • Pain
  • Pain Measurement
  • Patch-Clamp Techniques
  • Posterior Horn Cells
  • Prosencephalon
  • Receptors, N-Methyl-D-Aspartate
  • Synaptic Transmission
scroll to property group menus

Research

keywords

  • NMDA receptors
  • PSD-93
  • forebrain
  • persistent pain
  • spinal cord
  • surface expression
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0270-6474

PubMed ID

  • 12890763
scroll to property group menus

Additional Document Info

start page

  • 6703

end page

  • 6712

volume

  • 23

issue

  • 17

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support