ArticleNeurochemical research2013
Requirement of glycogenolysis for uptake of increased extracellular K+ in astrocytes: potential implications for K+ homeostasis and glycogen usage in brain.
Article in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
74 citing papers in PubMed, 119 citations in OpenAlex.
- Serendipitous compound action potential oscillations reveal glycolytic astrocyte and oxidative axon interstitial KExperimental physiology · 2026Article
- ZBTB7A-mediated regulation of astrocytic glycolysis in neurodegenerative diseases: insights from literature review and bioinformatics prediction.Frontiers in aging neuroscience · 2026Review
- Orchestrating brain fluid dynamics: circadian regulation of CSF, glymphatic exchange, and waste clearance.Frontiers in cell and developmental biology · 2026Review
- Adeno-Associated Virus-Based Gene Therapy for Lafora Disease inInternational journal of molecular sciences · 2025Article
- Old player, new roles: defining the role of the plastidial phosphorylase.The New phytologist · 2025Review
- Neural Metabolic Networks: Key Elements of Healthy Brain Function.Journal of neurochemistry · 2025Review
- 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
- The Role of Astrocytes in Migraine with Cortical Spreading Depression: Protagonists or Bystanders? A Narrative Review.Pain and therapy · 2024Review
- Brain energy metabolism: A roadmap for future research.Journal of neurochemistry · 2024Review
- The multifaceted roles of the brain glycogen.Journal of neurochemistry · 2024Review
- Role of Astrocytes in the Pathophysiology of Lafora Disease and Other Glycogen Storage Disorders.Cells · 2023Review
- The Effect of Inhibition of Perisynaptic Astrocyte Glycogen Utilization on Depression-Like Behavior.Turk psikiyatri dergisi = Turkish journal of psychiatry · 2023Article
- Glial Contributions to Lafora Disease: A Systematic Review.Biomedicines · 2022Review
- Cortical spreading depression can be triggered by sensory stimulation in primed wild type mouse brain: a mechanistic insight to migraine aura generation.The journal of headache and pain · 2022Article
- Time-dependent changes in hippocampal and striatal glycogen long after maze training in male rats.Neurobiology of learning and memory · 2021Article
- Astrocyte Bioenergetics and Major Psychiatric Disorders.Advances in neurobiology · 2021Review
- Heterogeneity of Astrocytes in Grey and White Matter.Neurochemical research · 2021Review
- A thermodynamic function of glycogen in brain and muscle.Progress in neurobiology · 2020Article
- Review
- Loss of UGP2 in brain leads to a severe epileptic encephalopathy, emphasizing that bi-allelic isoform-specific start-loss mutations of essential genes can cause genetic diseases.Acta neuropathologica · 2020Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The importance of astrocytic K(+) uptake for extracellular K(+) ([K(+)](e)) clearance during neuronal stimulation or pathophysiological conditions is increasingly acknowledged. It occurs by preferential stimulation of the astrocytic Na(+),K(+)-ATPase, which has higher K(m) and V(max) values than its neuronal counterpart, at more highly increased [K(+)](e) with additional support of the cotransporter NKCC1. Triggered by a recent DiNuzzo et al. paper, we used administration of the glycogenolysis inhibitor DAB to primary cultures of mouse astrocytes to determine whether K(+) uptake required K(+)-stimulated glycogenolysis. KCl was increased by either 5 mM (stimulating only the Na(+),K(+)-ATPase) or 10 mM (stimulating both transporters) in glucose-containing saline media prepared to become iso-osmotic after the addition. DAB completely inhibited both uptakes, the Na(+),K(+)-ATPase-mediated by preventing Na(+) uptake for stimulation of its intracellular Na(+)-activated site, and the NKCC1-mediated uptake by inhibition of depolarization- and L-channel-mediated Ca(2+) uptake. Drugs inhibiting the signaling pathways involved in either of these processes also abolished K(+) uptake. Assuming similar in vivo characteristics, partly supported by literature data, K(+)-stimulated astrocytic K(+) uptake must discontinue after normalization of extracellular K(+). This will allow Kir1.4-mediated release and reuptake by the less powerful neuronal Na(+),K(+)-ATPase.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.