Ketoprofen, a non-steroidal anti-inflammatory drug prevents the late-onset reduction of muscarinic receptors in gerbil hippocampus after transient forebrain ischemia

Masato Asanuma, Sakiko N. Asanuma, Marvin Gómez-Vargas, Mitsutoshi Yamamoto, Norio Ogawa

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Ischemia-induced hippocampal late-onset reduction of muscarinic acetylcholine receptors (LORMAR) begins as late as 7 days after transient forebrain ischemia in the gerbil, but it precedes to completion of neuronal death in the CA1 region. We previously reported that post-ischemic administration of cyclosporin A prevented LORMAR with suppression of astroglial and microglial activation. In the present study, we showed that the chronic post-ischemic administration of a non-steroidal anti-inflammatory drug, ketoprofen (5 mg/kg, subcutaneously, twice a day for 14 days) significantly reduced LORMAR both 14 days and 21 days after the 5-min transient ischemia. This protective effect of ketoprofen against LORMAR suggests that the non-steroidal anti-inflammatory drugs is clinically efficacious in the treatment of LORMAR, a sequela of cerebral ischemia.

Original languageEnglish
Pages (from-to)109-112
Number of pages4
JournalNeuroscience Letters
Volume225
Issue number2
DOIs
Publication statusPublished - Apr 4 1997

Keywords

  • Hippocampus
  • Ketoprofen
  • Late-onset damage
  • Muscarinic acetylcholine receptor
  • Non-steroidal anti-infalmmatory drug (NSAID)
  • Transient forebrain ischemia

ASJC Scopus subject areas

  • Neuroscience(all)

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