Abstract text (incl. figure legends and references)

Purpose

To determine the effect of capsaicin to central nervous system, we prepared morphologic changes and biochemical assay were investigated in mouse primary cultured CNS neuron.

Methods

The susceptability of capsaicin differs for different brain area. Cerebral cortex and hippocampus were more sensitive, and striatum, thalamus and midbrain area were less sensitive to capsaicinsusceptability. After capsaicin treatment, cortical and hippocampal neurons were died in dose-and time-dependent manner. By observation of nuclear fragmentation of capsaicin treated neuron, it is thought that the type of cell death is apoptosis rather than necrosis. The capsaicin receptor immunoreactive cells were observed in the cortex and hippocampus.It is consistent with area of damaged neuron. In case of capsaicin treated neurons, NOS activity stain was positive , the product of nitrite and anti-nitrotyrosineimmunoreactivity were increased, and agmatine, which is a competitive nitric oxide synthases (NOSs) inhibitor significantly protect cortical and hippocampal neurons from capsaicin-induced apoptosis.

Results

These results indicated that capsaicin induced influx of cation ions. These results showed that capsaicin induced influx of Ca2+, followed by neuronal NOS is activated by Ca2+ and induced cell death. Also, the activity of caspase 3 was increased after capsacin treatment in the cortical and hippocampal neurons.

Conclusions

These results demonstrate that capsaicin induced the apoptosis through acting with capsaicin receptors. Calcium influx due to capsaicin recptor activation may induce apoptosis, which is triggered the formation of peroxynitrite by activating NOS activity or is mediated by activating caspase 3 pathway.