ArticleNeurochemical research2014
Basic mechanism leading to stimulation of glycogenolysis by isoproterenol, EGF, elevated extracellular K+ concentrations, or GABA.
Article in Neurochemical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
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- A Bird's-Eye View of Glycolytic Upregulation in Activated Brain: The Major Fate of Lactate Is Release From Activated Tissue, Not Shuttling to Nearby Neurons.Journal of neurochemistry · 2025Review
- Beyond the heart: a review exploring non-cardiovascular effects of vasoactive agents.Frontiers in pharmacology · 2025Review
- Epidermal Growth Factor in the CNS: A Beguiling Journey from Integrated Cell Biology to Multiple Sclerosis. An Extensive Translational Overview.Cellular and molecular neurobiology · 2022Review
- Wdfy3 regulates glycophagy, mitophagy, and synaptic plasticity.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Neuromodulation of Glial Function During Neurodegeneration.Frontiers in cellular neuroscience · 2020Article
- Norepinephrine stimulates glycogenolysis in astrocytes to fuel neurons with lactate.PLoS computational biology · 2018Article
- Severe Convulsions and Dysmyelination in Both Jimpy and Cx32/47Neurochemical research · 2017Review
- Integration between Glycolysis and Glutamate-Glutamine Cycle Flux May Explain Preferential Glycolytic Increase during Brain Activation, Requiring Glutamate.Frontiers in integrative neuroscience · 2017Review
- Astrocyte Cultures Mimicking Brain Astrocytes in Gene Expression, Signaling, Metabolism and KNeurochemical research · 2017Article
- Role of the Astrocytic Na(+), K(+)-ATPase in K(+) Homeostasis in Brain: K(+) Uptake, Signaling Pathways and Substrate Utilization.Neurochemical research · 2015Review
- Astrocytic glycogenolysis: mechanisms and functions.Metabolic brain disease · 2015Review
- Sequential Astrocytic 5-HT2B Receptor Stimulation, [Ca(2+)]i Regulation, Glycogenolysis, Glutamate Synthesis, and K(+) Homeostasis are Similar but Not Identical in Learning and Mood Regulation.Frontiers in integrative neuroscience · 2015Article
- Chronic SSRI stimulation of astrocytic 5-HT2B receptors change multiple gene expressions/editings and metabolism of glutamate, glucose and glycogen: a potential paradigm shift.Frontiers in behavioral neuroscience · 2015Review
- Antagonists of the Vasopressin V1 Receptor and of the β(1)-Adrenoceptor Inhibit Cytotoxic Brain Edema in Stroke by Effects on Astrocytes - but the Mechanisms Differ.Current neuropharmacology · 2014Article
- Serotonin mediation of early memory formation via 5-HT2B receptor-induced glycogenolysis in the day-old chick.Frontiers in pharmacology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycogenolysis, in brain parenchyma an astrocyte-specific process, has changed from being envisaged as an emergency procedure to playing central roles during brain response to whisker stimulation, memory formation, astrocytic K(+) uptake and stimulated release of ATP. It is activated by several transmitters and by even very small increases in extracellular K(+) concentration, and to be critically dependent upon an increase in free cytosolic Ca(2+) concentration ([Ca(2+)]i), whereas cAMP plays only a facilitatory role together with increased [Ca(2+)]i. Detailed knowledge about the signaling pathways eliciting glycogenolysis is therefore of interest and was investigated in the present study in well differentiated cultures of mouse astrocytes. The β-adrenergic agonist isoproterenol stimulated glycogenolysis by a β1-adrenergic effect, which initiated a pathway in which cAMP/protein kinase A activated a Gi/Gs shift, leading to Ca(2+)-activated glycogenolysis. Inhibition of this pathway downstream of cAMP but upstream of the Gi/Gs shift abolished the glycogenolysis. However, inhibitors operating downstream of the Ca(2+)-sensitive step, but preventing transactivation-mediated epidermal growth factor (EGF) receptor stimulation, a later step in the activated pathway, also caused inhibition of glycogenolysis. For this reason the effect of EGF was investigated and it was found to be glycogenolytic. Large increases in extracellular K(+) activated glycogenolysis by a nifedipine-inhibited L-channel opening allowing influx of Ca(2+), known to be glycogenolysis-dependent. Small increases (addition of 5 mM KCl) caused a smaller effect by a similarly glycogenolysis-reliant opening of an IP3 receptor-dependent ouabain signaling pathway. The same pathway could be activated by GABA (also in brain slices) due to its depolarizing effect in astrocytes.
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