The glycogen, glucose and lactic acid content of the brain in experimental catatonia

Crossland, James; Rogers, Kathryn E.

doi:10.1016/0006-2952(68)90225-6

Cited by 12 publications

(2 citation statements)

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“…Presumably, readily mobilizable stores of glycogen combined with low cerebral metabolic requirements (Thurston and McDougal, 1969;Duffy et al, 1975) underlie the known tolerance of immature animals to hypoxic stress. The fractions of "free" and "bound" glycogen existed in newborn rat brain in a ratio of 1:2; a similar relationship has been observed in adult rat brain (Merrick, 1961;Crossland and Rogers, 1968;Nahorski et al, 1970). Total brain glycogen extracted by acid hydrolysis yielded values equivalent to 85% of the metabolite assayed with glucosidase.…”

Section: Discussionsupporting

confidence: 67%

“…Such overestimation, in turn, would serve to minimize the relative contribution of glycogen to cerebral energy supply during anoxia. gen fraction (Crossland and Rogers, 1968;Nahorski et al, 1970). The reason for this apparent agespecific discrepancy is unexplained but may relate to inherent differences in physicochemical properties of bound glycogen that make it more readily mobilizable in the immature animal.…”

Section: Discussionmentioning

confidence: 99%

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Glycogen Metabolism in Neonatal Rat Brain During Anoxia and Recovery

Vannucci

1980

Journal of Neurochemistry

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Metabolic alterations in glycogen and in glycogen-related metabolites were studied in neonatal rat brain during controlled anoxia and recovery. One-day postnatal rats were exposed to 100% N, at 37°C for up to 20 min; some rats were allowed to recover in air. Animals were frozen in liquid N, and the brains were prepared for fluorometric analysis of compounds involved in glycogen turnover. During anoxia, glycogen decreased by 29% and 42% at 10 and 20 min, respectively; the free (soluble) and bound (insoluble) components of glycogen decreased in nearly equal proportions. Brain glucose decreased by 72% at 10 min with little further change thereafter; G-6-P, G-I-P, and UDPG also declined. During recovery from anoxia, glucose and G-6-P increased above control levels for up to 60 min. G-1-P paralleled G-6-P levels, but UDPG remained low. Glycogen returned to control values by 4 h. The findings suggest that although glycogen is mobilized slowly in newborn rat brain, the metabolite contributes at least one-third of the cerebral energy supply during anoxia.Presumably, readily available stores of glycogen combined with low cerebral metabolic requirements underscore the known tolerence of immature animals to hypoxic stress. Glycogen accumulation during recovery appears to be facilitated at the synthetase step, since equilibrium measurements of the phosphoglucomutase and pyrophosphorylase systems indicate that these reactions are not rate-limiting for glycogen synthesis.

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