Possible involvement of nitric oxide in quinolinic acid-induced convulsion in mice

Toshi Aki Nakamura, Kiyofumi Yamada, Takaaki Hasegawa, Toshitaka Nabeshima

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26 Citations (Scopus)


Quinolinic acid (QA) induced clonic and tonic convulsions in mice when it was injected into the cerebral ventricle. Pretreatment with l-arginine (L-Arg), a substrate of nitric oxide (NO) synthase (NOS), and/or 5,6,7,8-tetrahydrobiopterin (THB), a cofactor of NOS, tended to potentiate QA-induced convulsion. NG-monomethyl-l-arginine (NMMA), a competitive NOS inhibitor, diminished QA-induced convulsion. This effect of NMMA was attenuated by coadministration of L-Arg or THB. Sodium nitroprusside (SNP), which spontaneously releases NO, did not potentiate, but diminished QA-induced convulsion. These findings suggest that an endogenous NO may be involved, at least in part, in QA-induced convulsion in mice, and that an exogenous NO released from SNP may cause downregulation of N-methyl-D-aspartate (NMDA) receptor activity, and thereby prevent the excessive excitation of NMDA receptors and subsequent convulsion caused by QA.

Original languageEnglish
Pages (from-to)309-312
Number of pages4
JournalPharmacology, Biochemistry and Behavior
Issue number2-3
Publication statusPublished - 1995
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Toxicology
  • Pharmacology
  • Clinical Biochemistry
  • Biological Psychiatry
  • Behavioral Neuroscience


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