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The rate of fall of the glycogen was linear during the period of aglycemia. This recommended 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 charge. Glycogen may 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 an element of about two compared to baseline ranges, the place the nerve is incubated in 10 mM glucose for 2 h (Wender et al., 2000). Exposing the optic nerve to aglycemia after growing glycogen content did certainly result in an increase within the latency to CAP failure. Incubating nerves in growing concentrations of glucose such that quite a lot of glycogen levels were attained resulted in a linear relationship whereby the latency to CAP failure was determined by the glycogen content, i.e., rising glycogen content in the nerve on the onset of aglycemia prolonged the latency to CAP failure.
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