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Related Concept Videos

Propagation of Action Potentials01:23

Propagation of Action Potentials

The propagation of an action potential refers to the process by which a nerve impulse, or "action potential," travels along a neuron.
Neurons (nerve cells) have a resting membrane potential, with a slightly negative charge inside compared to outside. This is maintained by ion channels, such as sodium (Na+) and potassium (K+) channels, which control the flow of ions. When a stimulus, like a touch or a signal from another neuron, triggers the neuron, sodium channels open, allowing sodium ions to...

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Updated: Jun 29, 2026

Real-time Electrophysiology: Using Closed-loop Protocols to Probe Neuronal Dynamics and Beyond
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Published on: June 24, 2015

Metabolic constraints shape hypersynchronous dynamics in spiking cortical microcircuit models.

Daniel Dadras1,2, Hae-Jeong Park3,4,5,6

  • 1Faculty of Medicine, Goethe University Frankfurt, Frankfurt am Main, Germany.

Scientific Reports
|June 27, 2026
PubMed
Summary
This summary is machine-generated.

Impaired brain energy metabolism can trigger seizure-like network activity. Computational models reveal how reduced ATP destabilizes cortical circuits, leading to synchronized bursting, and how inhibition can suppress this activity without restoring energy levels.

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Area of Science:

  • Computational Neuroscience
  • Systems Neuroscience
  • Neuroenergetics

Background:

  • Neuronal function relies on ATP-dependent ion homeostasis.
  • Understanding how metabolic stress impacts large-scale cortical network dynamics is challenging.
  • Existing seizure models lack direct links between cellular energy and network activity.

Purpose of the Study:

  • To investigate if reduced intracellular energy availability can destabilize cortical activity and induce seizure-like synchronization.
  • To develop a computational framework linking energy metabolism to neuronal excitability and network dynamics.
  • To explore the effects of metabolic stress on cortical network stability and seizure generation.

Main Methods:

  • Extended the Adaptive Exponential Integrate-and-Fire model with an energy variable.
  • Incorporated explicit ATP production and consumption terms.
  • Fitted layer-specific parameters to human cortical recordings and embedded the model in a laminar microcircuit.

Main Results:

  • Reduced ATP production induced a shift from asynchronous activity to a burst-synchronized state with low firing rates and high-amplitude oscillations.
  • Increased inhibitory conductance suppressed burst synchrony under metabolic stress but did not restore the metabolic state.
  • Parameter sweeps indicated history-dependent changes in burst synchrony, particularly with inhibitory modulation.

Conclusions:

  • Coupling intracellular energy availability to neuronal excitability is sufficient to destabilize cortical networks and generate seizure-like activity.
  • Inhibition can suppress seizure-like activity in a low-energy state, highlighting a distinction between electrical suppression and metabolic recovery.
  • The developed spiking-network model provides a framework for studying metabolic constraints on cortical stability and seizure dynamics.