Protection against kainate neurotoxicity by pyrrolidine dithiocarbamate

Eun Joo Shin, Jin Hyeong Jhoo, Won-Ki Kim, Wang Kee Jhoo, Chaeyoung Lee, Bae Dong Jung, Hyoung Chun Kim

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

1. The effect of pyrrolidine dithiocarbamate (PDTC) on kainate (KA)-induced neurotoxicity was examined in Sprague-Dawley rats. 2. At 10 mg/kg, i.p., KA produced seizures accompanied by neuronal loss in the hippocampus and increased levels of malondialdehyde (MDA) and protein carbonyl. 3. Pretreatment with PDTC (100 or 200 mg/kg, p.o., every 12 h x5) blocked KA-induced neurotoxicities (seizures, increases in MDA and protein carbonyl and neuronal losses) in a dose-dependent manner. These effects were counteracted by the adenosine A 1 receptor antagonist 8-cyclopentyl-1,3-dimetliylxanthine (25 or 50 μg/kg, i.p.), but not by the A2A receptor antagonist 1,3,7-trimethyl-8-(3-chlorostyryl)xanthine (0.5 or 1 mg/kg, i.p.) or the A 2B receptor antagonist alloxazine (1.5 or 3.0 mg/kg, i.p.). 4. Our results suggest that the anticonvulsant and neuroprotective effects of PDTC are mediated, at least in part, via adenosine A1 receptor stimulation.

Original languageEnglish
Pages (from-to)320-326
Number of pages7
JournalClinical and Experimental Pharmacology and Physiology
Volume31
Issue number5-6
DOIs
Publication statusPublished - 2004 May 1
Externally publishedYes

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Keywords

  • Adenosine A receptor
  • Anti-oxidant
  • Anticonvulsant effects
  • Hippocampus
  • Kainic acid
  • Malondialdehyde
  • Neuroprotective effects
  • Protein carbonyl
  • Pyrrolidine dithiocarbamate

ASJC Scopus subject areas

  • Physiology
  • Pharmacology (medical)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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