ArticleGlia2015
GABAergic disinhibition and impaired KCC2 cotransporter activity underlie tumor-associated epilepsy.
Article in Glia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
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Who cites it
120 citing papers in PubMed.
- Gliomas phenocopy an inborn error of metabolism to drive neuronal activity and tumor growth.Cell · 2026Article
- Restoration of gamma-aminobutyric acid homeostasis: A novel approach to alleviating central nervous system injury-associated immunodepression syndrome.Neural regeneration research · 2026Article
- Combined patch-clamp electrophysiology and single-cell genomic analysis reveal spiking tumor cells at the neocortical glioblastoma interface in humans.Neuro-oncology · 2026Article
- Transsynaptic tracing techniques to interrogate neuronal connectivity of glioblastomas.Nature protocols · 2026Review
- Leveraging neuroscience imaging and electrophysiological assessments to decode neuron-glioma interactions.Neuro-oncology advances · 2026Review
- Cancer neuroscience: signaling pathways and new therapeutic strategies for cancer.Signal transduction and targeted therapy · 2026Review
- Cancer Neuroscience: Linking Neuronal Plasticity with Brain Tumor Growth and Resistance.Biology · 2026Review
- Pathological neural and immune synapses in glioblastoma progression: mechanisms and therapeutic opportunities.Frontiers in neural circuits · 2026Review
- Decoding autophagy in neuro-tumor crosstalk: from underlying mechanisms to translational opportunities.Theranostics · 2026Review
- Exploring the Neurobiological Mechanisms of Cancer Growth.Current pharmaceutical design · 2026Review
- Neuron-Glioma Synapses in Tumor Progression.Biomedicines · 2025Review
- Serotonergic neuron-glioma interactions drive high-grade glioma pathophysiology.bioRxiv : the preprint server for biology · 2025Article
- Aberrant neural activity in the peritumoral cortex underlies the progression of tumor-associated seizures.Nature communications · 2025Article
- Neuroscience in glioma biology (Review).Oncology reports · 2025Review
- Circulating levels of glutamate predict brain disease in patients with advanced lung and breast cancer: a prospective study.Journal of neuro-oncology · 2025Observational
- Novel GABAAR antagonists target networked gene hubs at the leading edge in high-grade gliomas.Neuro-oncology · 2025Article
- Reprogramming neural-tumor crosstalk: emerging therapeutic dimensions and targeting strategies.Military Medical Research · 2025Review
- Cancer Neuroscience: Decoding Neural Circuitry in Tumor Evolution for Targeted Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Tumor-related epilepsy in glioma: A multidisciplinary overview.Epilepsia · 2025Review
- Research progress in glioma-related epilepsy (Review).Biomedical reports · 2025Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Seizures frequently accompany gliomas and often escalate to peritumoral epilepsy. Previous work revealed the importance of tumor-derived excitatory glutamate (Glu) release mediated by the cystine-glutamate transporter (SXC) in epileptogenesis. We now show a novel contribution of GABAergic disinhibition to disease pathophysiology. In a validated mouse glioma model, we found that peritumoral parvalbumin-positive GABAergic inhibitory interneurons are significantly reduced, corresponding with deficits in spontaneous and evoked inhibitory neurotransmission. Most remaining peritumoral neurons exhibit elevated intracellular Cl(-) concentration ([Cl(-) ]i ) and consequently depolarizing, excitatory gamma-aminobutyric acid (GABA) responses. In these neurons, the plasmalemmal expression of KCC2, which establishes the low [Cl(-) ]i required for GABAA R-mediated inhibition, is significantly decreased. Interestingly, reductions in inhibition are independent of Glu release, but the presence of both decreased inhibition and decreased SXC expression is required for epileptogenesis. We suggest GABAergic disinhibition renders peritumoral neuronal networks hyper-excitable and susceptible to seizures triggered by excitatory stimuli, and propose KCC2 as a therapeutic target.
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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.