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Acute Effects of Pyrethroids on Serotonin Release in the Striatum of Awake Rats: An In Vivo Microdialysis Study

Authors

  • Muhammad M. Hossain,

    Corresponding author
    1. Department of Veterinary Pharmacology, Faculty of Agriculture, Iwate University, Morioka, Japan
    • Department of Environmental and Occupational Medicine and Environmental and Occupational Health Sciences Institute, UMDNJ–Robert Wood Johnson Medical School, Piscataway, NJ, USA
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  • Tadahiko Suzuki,

    1. Department of Veterinary Pharmacology, Faculty of Agriculture, Iwate University, Morioka, Japan
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  • Jason R. Richardson,

    1. Department of Environmental and Occupational Medicine and Environmental and Occupational Health Sciences Institute, UMDNJ–Robert Wood Johnson Medical School, Piscataway, NJ, USA
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  • Haruo Kobayashi

    1. Department of Veterinary Pharmacology, Faculty of Agriculture, Iwate University, Morioka, Japan
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Correspondence to: Muhammad M. Hossain.

ABSTRACT

The present study examined the acute neurotoxic effects of three different pyrethroids, allethrin, cyhalothrin, and deltamethrin on the release of serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the striatum of conscious rats using microdialysis. Allethrin 10 mg/kg reduced extracellular levels of 5-HT to 46%, whereas 20 and 60 mg/kg increased the release to 177% and 243% of baseline, respectively. Cyhalothrin increased 5-HT release to 145–204% and deltamethrin decreased to 58–32% of baseline in a dose-dependent manner. None of the pyrethroids tested altered extracellular levels of 5-HIAA. Local infusion of the voltage-gated sodium channel antagonist tetrodotoxin (TTX) into striatum completely prevented the effects of allethrin, cyhalothrin, and deltamethrin (10 and 20 mg/kg) on 5-HT release. The effect of deltamethrin at 60 mg/kg was completely abolished by striatal infusion of nimodipine (L-type Ca++ channel antagonist) with TTX. These findings suggest that pyrethroids disrupt the serotonergic neurotransmission in striatum in a dose-related manner with Na+ and Ca2+ channel-dependent mechanisms. © 2012 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:150-156, 2013; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.21450

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