Nicotine upregulates nerve growth factor expression and prevents apoptosis of cultured spinal cord neurons

Rosario Garrido, Kelley King-Pospisil, Kwang Won Son, Bernhard Hennig, Michal Toborek

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


Modulation of neurotrophic factor expression may constitute an important part of neuroprotective effects of nicotine. Therefore, the effects of nicotine on expression of nerve growth factor (NGF) and its receptor, tyrosine receptor kinase A (trkA), were studied in cultured spinal cord neurons treated with arachidonic acid. Because injury to spinal cord is associated with elevated levels of arachidonic acid, this cell culture system has been developed in our laboratory as an in vitro model of neuronal injury in spinal cord trauma. Treatment with nicotine markedly upregulated NGF mRNA and protein expression in spinal cord neurons. In addition, a 12h treatment with nicotine increased mRNA levels of trkA. Both nicotine and exogenous NGF inhibited arachidonic acid induced apoptosis of spinal cord neurons. However, the blockage of the trkA receptor prevented nicotine-mediated anti-apoptotic effects. The present results indicate that increased expression of NGF may be an important element of the neuroprotective effects of nicotine in injured spinal cord neurons.

Original languageEnglish
Pages (from-to)349-355
Number of pages7
JournalNeuroscience Research
Issue number3
StatePublished - Nov 1 2003

Bibliographical note

Funding Information:
This work was supported in part by the Kentucky Spinal Cord and Head Injury Research Trust (KSCHIRT) and Philip Morris External Research Program.


  • Fatty acids
  • Neuroprotection
  • Nicotine
  • Spinal cord neurons
  • Spinal cord trauma

ASJC Scopus subject areas

  • General Neuroscience


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