ArticlePLoS computational biology2013
Divide and conquer: functional segregation of synaptic inputs by astrocytic microdomains could alleviate paroxysmal activity following brain trauma.
Article in PLoS computational biology, 2013. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Network effects of traumatic brain injury: from infra slow to high frequency oscillations and seizures.Journal of computational neuroscience · 2025Article
- Refractory density model of cortical direction selectivity: Lagged-nonlagged, transient-sustained, and On-Off thalamic neuron-based mechanisms and intracortical amplification.PLoS computational biology · 2020Article
- Dual roles of astrocytes in plasticity and reconstruction after traumatic brain injury.Cell communication and signaling : CCS · 2020Review
- Ionic and synaptic mechanisms of seizure generation and epileptogenesis.Neurobiology of disease · 2019Review
- A Theoretical Study on the Role of Astrocytic Activity in Neuronal Hyperexcitability by a Novel Neuron-Glia Mass Model.Journal of mathematical neuroscience · 2016Article
- Age dependency of trauma-induced neocortical epileptogenesis.Frontiers in cellular neuroscience · 2013Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Traumatic brain injury often leads to epileptic seizures. Among other factors, homeostatic synaptic plasticity (HSP) mediates posttraumatic epileptogenesis through unbalanced synaptic scaling, partially compensating for the trauma-incurred loss of neural excitability. HSP is mediated in part by tumor necrosis factor alpha (TNFα), which is released locally from reactive astrocytes early after trauma in response to chronic neuronal inactivity. During this early period, TNFα is likely to be constrained to its glial sources; however, the contribution of glia-mediated spatially localized HSP to post-traumatic epileptogenesis remains poorly understood. We used computational model to investigate the reorganization of collective neural activity early after trauma. Trauma and synaptic scaling transformed asynchronous spiking into paroxysmal discharges. The rate of paroxysms could be reduced by functional segregation of synaptic input into astrocytic microdomains. Thus, we propose that trauma-triggered reactive gliosis could exert both beneficial and deleterious effects on neural activity.
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Registered trials
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