Robust glycogen shunt activity in astrocytes: Effects of glutamatergic and adrenergic agents

Walls, Anne B.; Heimburger, C.; Bouman, Stephan D.; Schousboe, Arne; Waagepetersen, Helle S.

doi:10.1016/j.neuroscience.2008.09.058

Cited by 128 publications

(143 citation statements)

References 56 publications

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“…Glycogen may be converted to lactate that can be released to the extracellular space and used by neurons or other cells as fuel (20,21). Further, glycogen degradation fuels glutamate transport in astrocytes (11,22) or glycogen in astrocytes can be used for synthesis of glutamine, thus serving as precursor for biosynthesis of neurotransmitter glutamate (13). In line with this, it has been suggested that reduced glycogen degradation contributes to the imbalance of glutamatergic and GABAergic neurotransmission associated with epilepsy and seizures (24).…”

Section: Implication Of Glycogen In Seizuresmentioning

confidence: 95%

“…This may be explained by excessive neuronal activity being associated with efflux of K + which is subsequently removed from the extracellular space by active transport into astrocytes (23). In primary astrocyte cultures glycogen is involved in fueling the removal of K + from the extracellular space (11) and in line with this, it has been suggested that glucose is spared for neuronal energy metabolism when glycogen is used for fueling astrocytic K + clearance (27). In conclusion, altered glycogen metabolism seems to be clearly involved in seizure activity and epilepsy although the two scenarios appear to affect glycogen metabolism differently.…”

Section: Implication Of Glycogen In Seizuresmentioning

confidence: 99%

“…one instead of two ATP. However, despite being energetically unfavorable, glycogen shunt activity appears to operate persistently in muscle as well as in brain (11,(62)(63)(64). During increases in cerebral energy demand, the astrocytic glycogen content will, however, decrease (5,(64)(65)(66)(67)(68).…”

Section: Glycogen Shunt Activitymentioning

confidence: 99%

“…Thus, a linkage exists between breakdown of glycogen and the neural plasticity involved in both learning and addiction. In addition, glycogen breakdown is essential for key astrocytic processes, such as uptake of K + and neurotransmitter glutamate, and the subsequent synthesis of glutamine as part of the glutamate-glutamine cycle (9)(10)(11). However, several details regarding the role and regulation of glycogen metabolism in physiology and pathology are still obscure.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Astrocytic glycogen metabolism in the healthy and diseased brain

Bak¹,

Walls²,

Schousboe

et al. 2018

Journal of Biological Chemistry

114

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Section: Implication Of Glycogen In Seizuresmentioning

confidence: 95%

Section: Implication Of Glycogen In Seizuresmentioning

confidence: 99%

Section: Glycogen Shunt Activitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Astrocytic glycogen metabolism in the healthy and diseased brain

Bak¹,

Walls²,

Schousboe

et al. 2018

Journal of Biological Chemistry

114

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“…Glycogen levels reflect a dynamic equilibrium between glycogen synthesis and degradation, i.e. glycogenolysis (22).…”

mentioning

confidence: 99%

Insulin and Insulin-like Growth Factor 1 (IGF-1) Modulate Cytoplasmic Glucose and Glycogen Levels but Not Glucose Transport across the Membrane in Astrocytes

Muhič

Vardjan

Chowdhury

et al. 2015

Journal of Biological Chemistry

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Background: Astrocytes contain glycogen, an energy buffer in the brain. Results: Stimulation with insulin and IGF-1 decreases cytosolic glucose concentration in astrocytes without affecting glucose entry across the astrocyte plasma membrane. Conclusion: Insulin and IGF-1 boost the process of glycogen formation. Significance: This is the first high temporal resolution measurement of the decrease of glucose levels in astrocytes resulting from insulin and IGF-1 stimulation.

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Why does the brain (not) have glycogen?

2011

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In the present paper we formulate the hypothesis that brain glycogen is a critical determinant in the modulation of carbohydrate supply at the cellular level. Specifically, we propose that mobilization of astrocytic glycogen after an increase in AMP levels during enhanced neuronal activity controls the concentration of glucose phosphates in astrocytes. This would result in modulation of glucose phosphorylation by hexokinase and upstream cell glucose uptake. This mechanism would favor glucose channeling to activated neurons, supplementing the already rich neuron-astrocyte metabolic and functional partnership with important implications for the energy compounds used to sustain neuronal activity. The hypothesis is based on recent modeling evidence suggesting that rapid glycogen breakdown can profoundly alter the short-term kinetics of glucose delivery to neurons and astrocytes. It is also based on review of the literature relevant to glycogen metabolism during physiological brain activity, with an emphasis on the metabolic pathways identifying both the origin and the fate of this glucose reserve.

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Robust glycogen shunt activity in astrocytes: Effects of glutamatergic and adrenergic agents

Cited by 128 publications

References 56 publications

Astrocytic glycogen metabolism in the healthy and diseased brain

Astrocytic glycogen metabolism in the healthy and diseased brain

Insulin and Insulin-like Growth Factor 1 (IGF-1) Modulate Cytoplasmic Glucose and Glycogen Levels but Not Glucose Transport across the Membrane in Astrocytes

Why does the brain (not) have glycogen?

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