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Research ArticleNeuropharmacology

Expression and Activity of Nitric Oxide Synthase Isoforms in Methamphetamine-Induced Striatal Dopamine Toxicity

Danielle M. Friend, Jong H. Son, Kristen A. Keefe and Ashley N. Fricks-Gleason
Journal of Pharmacology and Experimental Therapeutics February 2013, 344 (2) 511-521; DOI: https://doi.org/10.1124/jpet.112.199745
Danielle M. Friend
Interdepartmental Program in Neuroscience (D.M.F., K.A.K.) and Department of Pharmacology and Toxicology (J.H.S., K.A.K., A.N.F.), University of Utah, Salt Lake City, Utah
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Jong H. Son
Interdepartmental Program in Neuroscience (D.M.F., K.A.K.) and Department of Pharmacology and Toxicology (J.H.S., K.A.K., A.N.F.), University of Utah, Salt Lake City, Utah
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Kristen A. Keefe
Interdepartmental Program in Neuroscience (D.M.F., K.A.K.) and Department of Pharmacology and Toxicology (J.H.S., K.A.K., A.N.F.), University of Utah, Salt Lake City, Utah
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Ashley N. Fricks-Gleason
Interdepartmental Program in Neuroscience (D.M.F., K.A.K.) and Department of Pharmacology and Toxicology (J.H.S., K.A.K., A.N.F.), University of Utah, Salt Lake City, Utah
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Abstract

Nitric oxide is implicated in methamphetamine (METH)-induced neurotoxicity; however, the source of the nitric oxide has not been identified. Previous work has also revealed that animals with partial dopamine loss induced by a neurotoxic regimen of methamphetamine fail to exhibit further decreases in striatal dopamine when re-exposed to methamphetamine 7–30 days later. The current study examined nitric oxide synthase expression and activity and protein nitration in striata of animals administered saline or neurotoxic regimens of methamphetamine at postnatal days 60 and/or 90, resulting in four treatment groups: Saline:Saline, METH:Saline, Saline:METH, and METH:METH. Acute administration of methamphetamine on postnatal day 90 (Saline:METH and METH:METH) increased nitric oxide production, as evidenced by increased protein nitration. Methamphetamine did not, however, change the expression of endothelial or inducible isoforms of nitric oxide synthase, nor did it change the number of cells positive for neuronal nitric oxide synthase mRNA expression or the amount of neuronal nitric oxide synthase mRNA per cell. However, nitric oxide synthase activity in striatal interneurons was increased in the Saline:METH and METH:METH animals. These data suggest that increased nitric oxide production after a neurotoxic regimen of methamphetamine results from increased nitric oxide synthase activity, rather than an induction of mRNA, and that constitutively expressed neuronal nitric oxide synthase is the most likely source of nitric oxide after methamphetamine administration. Of interest, animals rendered resistant to further methamphetamine-induced dopamine depletions still show equivalent degrees of methamphetamine-induced nitric oxide production, suggesting that nitric oxide production alone in response to methamphetamine is not sufficient to induce acute neurotoxic injury.

Footnotes

  • This work was supported by the National Institutes of Health National Institute on Drug Abuse [Grants DA 013367 and DA 031523].

  • dx.doi.org/10.1124/jpet.112.199745.

  • Received September 7, 2012.
  • Accepted December 7, 2012.
  • Copyright © 2013 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 344 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 344, Issue 2
1 Feb 2013
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Research ArticleNeuropharmacology

NOS Isoforms in METH-Induced DA Toxicity

Danielle M. Friend, Jong H. Son, Kristen A. Keefe and Ashley N. Fricks-Gleason
Journal of Pharmacology and Experimental Therapeutics February 1, 2013, 344 (2) 511-521; DOI: https://doi.org/10.1124/jpet.112.199745

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Research ArticleNeuropharmacology

NOS Isoforms in METH-Induced DA Toxicity

Danielle M. Friend, Jong H. Son, Kristen A. Keefe and Ashley N. Fricks-Gleason
Journal of Pharmacology and Experimental Therapeutics February 1, 2013, 344 (2) 511-521; DOI: https://doi.org/10.1124/jpet.112.199745
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