Nicotine up‐regulates expression of neurotrophic factors and attenuates apoptosis of spinal cord neurons

Abstract

Nicotine may induce neuroprotection in spinal cord injury; however, the mechanisms of these effects are not fully understood. The present study focused on the effects of nicotine on expression of neurotrophic factors, such as brain‐derived neurotrophic factor (BDNF) and basic fibroblast growth factor (FGF‐2) in a model of spinal cord injury. In this model, cultured spinal cord neurons are exposed to 10 mm arachidonic acid (AA). Exposure to AA diminished expression of BDNF and FGF‐2; however, pretreatment with nicotine protected against these effects. Mecamylamine and α‐bungarotoxin inhibited nicotine‐mediated up‐regulation of BDNF and FGF‐2. Moreover, nicotine, BDNF and FGF‐2 protected against AA‐induced apoptosis of spinal cord neurons. These results suggest that AA can induce apoptosis of spinal cord neurons by depletion of neurotrophic factors and that nicotine can protect against these effects through the alpha7 receptor‐mediated pathway.Acknowledgements: Supported by grants from Philip Morris Research Program and KSCHIRT.