to proteoglycan sulfation. The rationale behind sodium chlorate’s possible benefits to axonal regeneration lie in its supposed ability to limit CSPG production. A ‘debunking’ of this notion would encourage researchers to explore other more promising options for limiting CSPGs, such as Chondroitinase ABC or Interferon-γ (Bradbury & Carter, 2011; Fujiyoshi et al., 2010). This experiment attempted to find a relationship between sodium chlorate and electrophysiological activity of spinal cord neurons. It was expected that sodium chlorate would block proteoglycan sulfation (Phamantu et al., 1999; Shannon et al., 2003), which would inhibit CSPG synthesis, which would in turn counteract the axon-inhibitory properties of CSPGs (Rhodes & Fawcett, 2004), leading to increased axonal regeneration, resulting in higher levels of electrophysiological activity being recorded from the MEAs. However, electrophysiological activity recorded from the regularly active MEAs did not show any statistically significant difference, regardless of exposure to sodium chlorate. Despite these results, future work is needed in order to conclude that sodium chlorate does not operate in the manner theorized. A group of 6 active MEAs (3 experimental and 3 controls) is recommended for future work, and the experimental group should be exposed to sodium chlorate during the entire cultivation period (immediately following plating). These measures will ideally provide a more significant set of data that reflects the impact, or lack thereof, that sodium chlorate has on electrophysiological activity of spinal cord neurons.
ACKNOWLEDGEMENTS This experiment was made possible through the use of resources from George Mason University’s Neural Engineering Lab, funded by an NSF grant. The authors want to thank Michael Maquera for his knowledge on conducting media exchanges and recording electric activity from cultures. Additionally, they want to thank Sharon Jose for her knowledge on MATLAB programming and data sorting.
96 | THE GEORGE MASON REVIEW