Sensory stimulation induces local cerebral glycogenolysis: Demonstration by autoradiography

Functional Astrocyte-Neuron Lactate Shuttle in a Human Stem Cell-Derived Neuronal Network

“…We also demonstrate that lactate production and glycogen breakdown occur in astrocytes after neuronal activation and hypoglycemia and is blocked using 1,4-dideoxy-1,4-imino-d-arabinitol. [34][35][36][37] These results, together with glycogen staining, suggest that NT2.A cells possess the machinery required for glycogen synthesis and glycogen breakdown. The decrease in glycogen levels and subsequent increase in lactate suggest that NT2.A respond to glutamate and potassium, not only by increasing glucose uptake, but also by degrading glycogen as demonstrated in vivo and in primary cultures.…”

“…The decrease in glycogen levels and subsequent increase in lactate suggest that NT2.A respond to glutamate and potassium, not only by increasing glucose uptake, but also by degrading glycogen as demonstrated in vivo and in primary cultures. [34][35][36]38 Treatments of co-cultures with dbcAMP and the b 1 and b 2 -adrenoreceptor agonist isoproterenol-induced glycogenolysis within astrocytes. dbcAMP activates glycogen phosphorylase through activation of protein kinase A leading to glycogen breakdown 39 while isoproterenol in turn acts by elevating levels of cyclic AMP.…”

Energy Metabolism in Astrocytes: High Rate of Oxidative Metabolism and Spatiotemporal Dependence on Glycolysis/Glycogenolysis

“…During a specific activation paradigm, such as sensory stimulation, glycogen breakdown (glycogenolysis), and oxidative metabolism in astrocytes increase in brain in situ (Swanson et al, 1992;Cruz et al, 2005; R Gruetter, presented at the Third Wierzba Conference, 2005). The response to activation is greater and more complex than that calculated on the basis of only the two adenosine 5 0 triphosphate (ATP)-dependent reactions involved in neurotransmitter glutamate-glutamine cycling (e.g., Attwell and Laughlin, 2001).…”

“…Astrocytes and neurons metabolize glucose via glycolytic, pentose shunt, and oxidative pathways, whereas only astrocytes have the ability to store glucose as glycogen, a high molecular-weight glucose polymer, in an energy-requiring process (Hamprecht et al, 2005). In brain, the glycogen level is stable under resting conditions and its turnover is slow (Watanabe and Passonneau, 1973;Choi et al, 2003), but glycogenolysis can increase substantially during brain activation (Swanson et al, 1992;Cruz and Dienel, 2002).Glucose enters the glycolytic pathway after phosphorylation by hexokinase to glucose-6-phosphate (G6P), and under resting conditions, about half of the phosphorylation of blood-borne glucose in brain of conscious rats in vivo occurs in astrocytes (Nehlig et al, 2004). Glucose-6-phosphate is also generated from glycogen after initial conversion of glucosyl units to glucose-1-phosphate (G1P) by glycogen phosphorylase.…”

Brain Glycogen Content and Metabolism in Subjects with Type 1 Diabetes and Hypoglycemia Unawareness

“…Another potential mechanism to enhance fuel availability during hypoglycemia is to increase brain glycogen content via a phenomenon termed 'supercompensation'. In the adult brain, glycogen is primarily localized in astrocytes (Wiesinger et al, 1997) and may support brain function either by being used locally in astrocytes, which would spare extracellular glucose for neurons, or by being exported to neurons in the form of lactate (Brown et al, 2005;Dienel et al, 2007;DiNuzzo et al, 2010;Sickmann et al, 2009;Swanson et al, 1992;Wender et al, 2000). Glycogen is mobilized during hypoglycemia both in rodents (Canada et al, 2011;Herzog et al, 2008;Suh et al, 2007) and in humans (Ö z et al, 2009).…”