Electrophysiological insights into glioma: From circuit disruption to therapeutic advances

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About this Research Topic

Submission deadlines

  1. Manuscript Submission Deadline 9 January 2026

  2. This Research Topic is currently accepting articles.

Background

Gliomas are among the most aggressive brain tumors, with glioblastoma offering a median survival of 12 to 15 months. Despite advances in surgical, radiological, and chemotherapeutic approaches, long-term prognosis remains poor. Evidence reveals that gliomas do not merely invade brain tissue but actively integrate into neural circuits. Recent research shows glioma cells infiltrate neighboring brain tissue and merge with pre-existing neuronal networks to create synaptic-like connections that use neural activity to support tumorous growth. Glioma patients frequently experience cognitive deficits and seizures from the bidirectional loop created by this synaptic crosstalk between tumor and brain, indicating involvement in local neural circuit function.

This Research Topic focuses on how electrophysiological approaches uncover mechanisms by which gliomas alter circuit function. Techniques like patch-clamp, in vivo electrophysiology, optogenetics, and neural interface technologies are increasingly used to dissect neuron–glioma interactions at cellular, synaptic, and network levels. Traditional models lack the resolution to represent dynamic tumor–circuit interactions, and the electrophysiological topography of brain regions invaded by gliomas remains poorly characterized. To better understand this vicious neuro-oncological loop, interdisciplinary approaches combining neurophysiology, cancer biology, and translational techniques are needed.

Gliomas have traditionally been studied through a tumor-centric lens, emphasizing genetic mutations, immune evasion, and invasive growth. However, recent insights have challenged this view, revealing that gliomas are not merely passive invaders but active participants in neural circuitry. High-grade gliomas, particularly glioblastomas, form functional glutamatergic synapses with neurons and hijack neuronal excitability to fuel tumor progression. This tumor–neuron crosstalk not only promotes proliferation but also disrupts both local and global brain network dynamics, leading to seizures, cognitive decline, and diminished quality of life.

Electrophysiological techniques provide real-time, high-resolution data on how gliomas alter neural function. Despite their potential, electrophysiological studies of tumor–circuit interfaces remain underutilized. Understanding the tumor–circuit interface is essential to developing interventions that not only slow progression but also preserve neural integrity and function.

This Research Topic highlights the crucial relationship between glioma biology and brain circuit function. We aim to bring together studies that clarify how gliomas disrupt neural activity, co-opt synaptic communication, and influence patient outcomes through electrophysiological approaches. Progress demands addressing key questions: How do glioma subtypes affect circuit excitability? Can electrophysiological markers predict tumor behavior or treatment response? Are certain neurons more vulnerable to tumor-induced hyperexcitability? By presenting novel methods and fostering dialogue, this collection seeks to define the circuit signature of glioma progression and uncover targets for preserving cognitive and neural integrity.

We invite contributions investigating glioma electrophysiological dynamics across molecular, synaptic, cellular, network, and behavioral scales. Contributions using organoids, human tissue, animal models, or computational approaches are welcome, particularly those integrating electrophysiology with molecular, imaging, or optogenetic data. Potential themes include:

• Neuron–glioma synaptic interactions
• Circuit dysfunction and hyperexcitability in glioma models
• Electrophysiological biomarkers for diagnosis or prognosis
• Tools integrating electrophysiology with imaging or optogenetics
• Translational studies aiming to restore circuit function
• Human tissue studies or organoid models exploring glioma activity
•Neuromodulation and circuit-targeted therapies

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Keywords: Glioma, DIPG, High-grade gliomas, Brain cancer, Synaptic communication, H3K27M mutation

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