Protection against kainate neurotoxicity by pyrrolidine dithiocarbamate
- Authors
- Shin E.-J.; Jhoo J.H.; Kim W.-K.; Jhoo W.K.; Lee C.; Jung B.D.; Kim H.-C.
- Issue Date
- 2004
- Keywords
- Adenosine A1 receptor; Anti-oxidant; Anticonvulsant effects; Hippocampus; Kainic acid; Malondialdehyde; Neuroprotective effects; Protein carbonyl; Pyrrolidine dithiocarbamate
- Citation
- Clinical and Experimental Pharmacology and Physiology, v.31, no.5-6, pp 320 - 326
- Pages
- 7
- Indexed
- SCOPUS
- Journal Title
- Clinical and Experimental Pharmacology and Physiology
- Volume
- 31
- Number
- 5-6
- Start Page
- 320
- End Page
- 326
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/20838
- DOI
- 10.1111/j.1440-1681.2004.03990.x
- ISSN
- 0305-1870
1440-1681
- 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.
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- Appears in
Collections - 1. Basic Science > Department of Neuroscience > 1. Journal Articles
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