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

11 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

Fingerprint

Ketoprofen
Gerbillinae
Muscarinic Receptors
Prosencephalon
Hippocampus
Anti-Inflammatory Agents
Ischemia
Pharmaceutical Preparations
Brain Ischemia
Cyclosporine

Keywords

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

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Ketoprofen, a non-steroidal anti-inflammatory drug prevents the late-onset reduction of muscarinic receptors in gerbil hippocampus after transient forebrain ischemia. / Asanuma, Masato; Asanuma, Sakiko N.; Gómez-Vargas, Marvin; Yamamoto, Mitsutoshi; Ogawa, Norio.

In: Neuroscience Letters, Vol. 225, No. 2, 04.04.1997, p. 109-112.

Research output: Contribution to journalArticle

@article{13b01d19c975436080676e658b8ad455,
title = "Ketoprofen, a non-steroidal anti-inflammatory drug prevents the late-onset reduction of muscarinic receptors in gerbil hippocampus after transient forebrain ischemia",
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.",
keywords = "Hippocampus, Ketoprofen, Late-onset damage, Muscarinic acetylcholine receptor, Non-steroidal anti-infalmmatory drug (NSAID), Transient forebrain ischemia",
author = "Masato Asanuma and Asanuma, {Sakiko N.} and Marvin G{\'o}mez-Vargas and Mitsutoshi Yamamoto and Norio Ogawa",
year = "1997",
month = "4",
day = "4",
doi = "10.1016/S0304-3940(97)00204-8",
language = "English",
volume = "225",
pages = "109--112",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "2",

}

TY - JOUR

T1 - Ketoprofen, a non-steroidal anti-inflammatory drug prevents the late-onset reduction of muscarinic receptors in gerbil hippocampus after transient forebrain ischemia

AU - Asanuma, Masato

AU - Asanuma, Sakiko N.

AU - Gómez-Vargas, Marvin

AU - Yamamoto, Mitsutoshi

AU - Ogawa, Norio

PY - 1997/4/4

Y1 - 1997/4/4

N2 - 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.

AB - 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.

KW - Hippocampus

KW - Ketoprofen

KW - Late-onset damage

KW - Muscarinic acetylcholine receptor

KW - Non-steroidal anti-infalmmatory drug (NSAID)

KW - Transient forebrain ischemia

UR - http://www.scopus.com/inward/record.url?scp=0031552371&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031552371&partnerID=8YFLogxK

U2 - 10.1016/S0304-3940(97)00204-8

DO - 10.1016/S0304-3940(97)00204-8

M3 - Article

C2 - 9147386

AN - SCOPUS:0031552371

VL - 225

SP - 109

EP - 112

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 2

ER -