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The rate of fall of the glycogen was linear throughout the period of aglycemia. This suggested that if glycogen was unregulated previous to introducing aglycemia then the latency to CAP failure may very well be extended 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 2 h increases the glycogen content by an element of about two compared to baseline ranges, where the nerve is incubated in 10 mM glucose for two h (Wender et al., 2000). Exposing the optic nerve to aglycemia after increasing glycogen content material did certainly result in a rise in the latency to CAP failure. Incubating nerves in growing concentrations of glucose such that a variety of glycogen ranges were attained resulted in a linear relationship whereby the latency to CAP failure was decided by the glycogen content material, i.e., rising glycogen content in the nerve at the onset of aglycemia prolonged the latency to CAP failure.
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