The speed of fall of the glycogen was linear throughout the period of aglycemia. This recommended that if glycogen was unregulated previous to introducing aglycemia then the latency to CAP failure could be prolonged if glycogen was metabolized at the identical steady fee. Glycogen might be unregulated by bathing the nerve in supra-physiological concentrations of glucose, thus incubating the nerve in 30 mM glucose for two h increases the glycogen content by an element of about two compared to baseline levels, the place the nerve is incubated in 10 mM glucose for two h (Wender et al., 2000). Exposing the optic nerve to aglycemia after growing glycogen content material did certainly lead to an increase in the latency to CAP failure. Incubating nerves in growing concentrations of glucose such that a variety of glycogen levels have been attained resulted in a linear relationship whereby the latency to CAP failure was determined by the glycogen content material, i.e., growing glycogen content in the nerve on the onset of aglycemia prolonged the latency to CAP failure.

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