Nicotine attenuates iNOS expression and contributes to neuroprotection in a compressive model of spinal cord injury

Mee Young Lee, Lei Chen, Michal J Toborek

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Primary impact to the spinal cord results in stimulation of secondary processes that potentiate the initial trauma. In the present study, we hypothesized that the altered expression of nitric oxide synthase (NOS) may contribute to these effects. Recent evidence indicates that nicotine can exert potent antioxidant and neuroprotective effects in spinal cord injury (SCI). Therefore, the aim of the present study was to evaluate whether the administration of nicotine can influence expression of inducible NOS (iNOS) and/or neuronal NOS (nNOS) in injured spinal cords. Adult male Long-Evans rats were subjected to a moderate contusion model of SCI and received a single intraperitoneal injection of either saline or nicotine (0.35, 3.5, or 7 mg/kg) 2 hr after trauma. SCI dramatically increased iNOS (but not nNOS) mRNA and protein levels in microglial cells in the thoracic and lumbar regions of spinal cords. iNOS overexpression resulted in increased nitrotyrosine formation, decreased number of NeuN (neuronal nuclei)-immunoreactive cells, and up-regulation of inflammatory genes. Most importantly, these effects were markedly attenuated by nicotine acting via a receptor-mediated mechanism. These data may have significant therapeutic implications for the targeting of nicotine receptors in the treatment of compressive spinal cord trauma.

Original languageEnglish
Pages (from-to)937-947
Number of pages11
JournalJournal of Neuroscience Research
Volume87
Issue number4
DOIs
StatePublished - Jun 1 2009
Externally publishedYes

Fingerprint

Spinal Cord Injuries
Nicotine
Spinal Cord
Lumbosacral Region
Long Evans Rats
Contusions
Wounds and Injuries
Neuroprotective Agents
Nitric Oxide Synthase Type II
Intraperitoneal Injections
Cell Nucleus
Nitric Oxide Synthase
Up-Regulation
Thorax
Antioxidants
Neuroprotection
Messenger RNA
Therapeutics
Genes
Proteins

Keywords

  • Inflammatory responses
  • Neuronal nicotinic receptors
  • Nicotine
  • Nitric oxide synthase
  • Oxidative stress
  • Spinal cord injury

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this

Nicotine attenuates iNOS expression and contributes to neuroprotection in a compressive model of spinal cord injury. / Lee, Mee Young; Chen, Lei; Toborek, Michal J.

In: Journal of Neuroscience Research, Vol. 87, No. 4, 01.06.2009, p. 937-947.

Research output: Contribution to journalArticle

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