ArticleNature communications2023
Mechanisms underlying pathological cortical bursts during metabolic depletion.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Article
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- Maturation of Neuronal Activity in the Human Cortex Exhibits Robust Spatial Gradients across the Birth Transition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Mechanisms and interventions promoting healthy frontostriatal dynamics in obsessive-compulsive disorder.Nature communications · 2025Article
- GABA-transaminase: A Key Player and Potential Therapeutic Target for Neurological Disorders.Central nervous system agents in medicinal chemistry · 2024Review
- Spontaneous activation of cortical somatosensory networks depresses their excitability in preterm human neonates.Imaging neuroscience (Cambridge, Mass.)Article
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cortical activity depends upon a continuous supply of oxygen and other metabolic resources. Perinatal disruption of oxygen availability is a common clinical scenario in neonatal intensive care units, and a leading cause of lifelong disability. Pathological patterns of brain activity including burst suppression and seizures are a hallmark of the recovery period, yet the mechanisms by which these patterns arise remain poorly understood. Here, we use computational modeling of coupled metabolic-neuronal activity to explore the mechanisms by which oxygen depletion generates pathological brain activity. We find that restricting oxygen supply drives transitions from normal activity to several pathological activity patterns (isoelectric, burst suppression, and seizures), depending on the potassium supply. Trajectories through parameter space track key features of clinical electrophysiology recordings and reveal how infants with good recovery outcomes track toward normal parameter values, whereas the parameter values for infants with poor outcomes dwell around the pathological values. These findings open avenues for studying and monitoring the metabolically challenged infant brain, and deepen our understanding of the link between neuronal and metabolic activity.
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Registered trials
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