The speed of fall of the glycogen was linear during the period of aglycemia. This steered that if glycogen was unregulated prior to introducing aglycemia then the latency to CAP failure could possibly be prolonged if glycogen was metabolized at the identical regular rate. Glycogen could be unregulated by bathing the nerve in supra-physiological concentrations of glucose, thus incubating the nerve in 30 mM glucose for two h will increase the glycogen content material by a factor of about two in comparison with baseline ranges, where the nerve is incubated in 10 mM glucose for 2 h (Wender et al., 2000). Exposing the optic nerve to aglycemia after rising glycogen content material did certainly lead to a rise within the latency to CAP failure. Incubating nerves in growing concentrations of
glucose balance support such that a wide range of glycogen ranges have been attained resulted in a linear relationship whereby the latency to CAP failure was determined by the glycogen content material, i.e., increasing glycogen content within the nerve on the onset of aglycemia prolonged the latency to CAP failure.
