PDZ domains at excitatory synapses: Potential molecular targets for persistent pain treatment

Yuan Xiang Tao, Roger A. Johns

Research output: Contribution to journalReview articlepeer-review

Abstract

Persistent pain, a common clinical condition, could be caused by inflammation, tissue injury secondary to trauma or surgery, and nerve injuries. It is often inadequately controlled by current treatments, such as opioids and non-steroidal anti-inflammatory drugs. The PDZ (Postsynaptic density 95, Discs large, and Zonula occludens-1) domains are ubiquitous protein interaction modules often found among multi-protein signaling complexes at neuronal synapses. Recent preclinical research shows that targeted disruption of PDZ domain-mediated protein interaction among N-methyl-Daspartate (NMDA) receptor signaling complexes significantly attenuates the development and maintenance of persistent pain without affecting nociceptive responsiveness to acute pain. PDZ domains at excitatory synapses may be new molecular targets for prevention and treatment of persistent pain. Here, we illustrate expression and distribution of the PDZ domain-containing proteins associated with NMDA receptors in the pain-related regions of the central nervous system, review the evidence for their roles in persistent pain states, and discuss potential mechanisms by which these PDZ domain-containing proteins are involved in persistent pain.

Original languageEnglish (US)
Pages (from-to)217-223
Number of pages7
JournalCurrent Neuropharmacology
Volume4
Issue number3
DOIs
StatePublished - Jul 2006

Keywords

  • AMBA receptors
  • Chronic pain
  • NMDA receptors
  • PSD-93
  • PSD-95
  • Persistent pain
  • Spinal cord
  • Trafficking

ASJC Scopus subject areas

  • Pharmacology
  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Pharmacology (medical)

Fingerprint Dive into the research topics of 'PDZ domains at excitatory synapses: Potential molecular targets for persistent pain treatment'. Together they form a unique fingerprint.

Cite this