ArticleFrontiers in cellular neuroscience2015
Augmentation of Ca(2+) signaling in astrocytic endfeet in the latent phase of temporal lobe epilepsy.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Astrocytes in Genetic Epilepsies: Supporting Actor or Key Player?Journal of neuroscience research · 2026Review
- The Role of Astrocytes in Migraine with Cortical Spreading Depression: Protagonists or Bystanders? A Narrative Review.Pain and therapy · 2024Review
- BubbleDrive, a low-volume incubation chamber for acute brain slices.Scientific reports · 2023Article
- Astrocyte-neuron circuits in epilepsy.Neurobiology of disease · 2023Review
- Review
- Reactive astrocyte-driven epileptogenesis is induced by microglia initially activated following status epilepticus.JCI insight · 2021Article
- Astrocytic CaFrontiers in cellular neuroscience · 2021Review
- Aquaporin-4-independent volume dynamics of astroglial endfeet during cortical spreading depression.Glia · 2019Article
- Conditional Knock-out of mGluR5 from Astrocytes during Epilepsy Development Impairs High-Frequency Glutamate Uptake.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Neuronal and glial DNA methylation and gene expression changes in early epileptogenesis.PloS one · 2019Article
- Ca2+ Signals in Astrocytes Facilitate Spread of Epileptiform Activity.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Blood DNA methylation pattern is altered in mesial temporal lobe epilepsy.Scientific reports · 2017Article
- Repeated low-dose kainate administration in C57BL/6J mice produces temporal lobe epilepsy pathology but infrequent spontaneous seizures.Experimental neurology · 2016Article
- Probing the Complexities of Astrocyte Calcium Signaling.Trends in cell biology · 2016Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocytic endfeet are specialized cell compartments whose important homeostatic roles depend on their enrichment of water and ion channels anchored by the dystrophin associated protein complex (DAPC). This protein complex is known to disassemble in patients with mesial temporal lobe epilepsy and in the latent phase of experimental epilepsies. The mechanistic underpinning of this disassembly is an obvious target of future therapies, but remains unresolved. Here we show in a kainate model of temporal lobe epilepsy that astrocytic endfeet display an enhanced stimulation-evoked Ca(2+) signal that outlast the Ca(2+) signal in the cell bodies. While the amplitude of this Ca(2+) signal is reduced following group I/II metabotropic receptor (mGluR) blockade, the duration is sustained. Based on previous studies it has been hypothesized that the molecular disassembly in astrocytic endfeet is caused by dystrophin cleavage mediated by Ca(2+) dependent proteases. Using a newly developed genetically encoded Ca(2+) sensor, the present study bolsters this hypothesis by demonstrating long-lasting, enhanced stimulation-evoked Ca(2+) signals in astrocytic endfeet.
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