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The speed of fall of the glycogen was linear through the interval of aglycemia. This urged that if glycogen was unregulated prior to introducing aglycemia then the latency to CAP failure might be prolonged if glycogen was metabolized at the same steady fee. Glycogen could be unregulated by bathing the nerve in supra-physiological concentrations of glucose, thus incubating the nerve in 30 mM glucose for 2 h will increase the glycogen content by an element of about two in comparison with 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 increasing glycogen content did indeed lead to a rise within the latency to CAP failure. Incubating nerves in growing concentrations of glucose such that quite a lot of glycogen ranges had been attained resulted in a linear relationship whereby the latency to CAP failure was determined by the glycogen content material, i.e., rising glycogen content material within the nerve on the onset of aglycemia prolonged the latency to CAP failure.
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