Apoptosis in Neuronal Populations of C. Elegans through Exposure to Caffeine

Abstract

Caffeine is the most widely used psychoactive drug in the world and forms a mild dependency in individuals who overuse the drug for an extended period. Other stimulant drugs, including methamphetamines, have been shown to induce apoptosis in the brain’s reward pathways, suggesting that stimulants may lead to apoptosis to lasting neuronal damage. Caffeine has been shown to induce apoptosis in gastric cancer cells in vitro as well as neonatal rat brain and cortical cell cultures. In C. elegans, the homolog of the p‐53 pathway is the CEP‐1 pathway. Caffeine induces apoptosis in human osteoblasts via the p53, Bax, and caspase 3 pathways. However, other studies suggest that caffeine produces inverse effects; caffeine exposure has been reported to increase longevity of Caenorhabditis elegans through activation of the IGF‐1 signaling pathway. Our current data clarifies the relationship between caffeine exposure and CEP‐1 via TG‐12, a C. elegans strain with CEP‐1:: GFP fusion gene.Here we discuss the results of caffeine exposure on TG‐12 worms. Early data indicates that exposure to high levels of caffeine leads to apoptosis in the nerve ring region of the worm. Here we attempt to identify the affected neuronal populations. We plan to further investigate the relationship between CEP‐1 and caffeine exposure in a dose‐dependent fashion via qRT‐PCR.Support or Funding InformationThis work was supported and funded by the Nueva School. The Shen Lab at Stanford University provided lab equipment and OH11061 worms. Worms and technical support were provided by Caenorhabditis Genetics Center (CGC) ‐ College of Biological Sciences