The beta-lactam antibiotic, ceftriaxone, inhibits the development of opioid-induced hyperalgesia in mice

Zhijun Chen, Ying He, Zaijie Jim Wang

Research output: Contribution to journalComment/debate

24 Scopus citations

Abstract

The glutamate transporter GLT-1 is primarily responsible for glutamate clearance in the spinal cord. beta-Lactam antibiotics have been shown to attenuate neuropathic pain behaviors by promoting GLT-1 expression and function in the CNS. The present study tested the hypothesis that ceftriaxone, a prototype beta-lactam antibiotic, can prevent the development of opioid-induced hyperalgesia (OIH) in mice. Repeated morphine administration produced mechanical allodynia and thermal hyperalgesia, signs of OIH, and reduced spinal GLT-1 expression in mice. Ceftriaxone (200. mg/kg/d, i.p., for 7 d) inhibited OIH. Correlating with the behavioral effects, ceftriaxone reversed downregulation of GLT-1 expression that was induced by OIH. These results suggest that ceftriaxone inhibited the development of OIH by up-regulating spinal GLT-1 expression.

Original languageEnglish
Pages (from-to)69-71
Number of pages3
JournalNeuroscience Letters
Volume509
Issue number2
DOIs
StatePublished - 16 Feb 2012
Externally publishedYes

Keywords

  • Allodynia
  • Beta-Lactam antibiotic
  • Ceftriaxone
  • GLT-1
  • Hyperalgesia
  • Opioid

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