Expansion of epileptogenic networks via neuroplasticity in neural mass models

Neuroplasticity refers to functional and structural changes in brain regions in response to healthy and pathological activity. Activity dependent plasticity induced by epileptic activity can involve healthy brain regions into the epileptogenic network by perturbing their excitation/inhibition balance. In this article, we present a new neural mass model, which accounts for neuroplasticity, for investigating the possible mechanisms underlying the epileptogenic network expansion. Our multiple-timescale model is inspired by physiological calcium-mediated synaptic plasticity and pathological extrasynaptic N-methyl-D-aspartate (NMDA) dependent plasticity dynamics. The model highlights that synaptic plasticity at excitatory connections and structural changes in the inhibitory system can transform a healthy region into a secondary epileptic focus under recurrent seizures and interictal activity occurring in the primary focus. Our results suggest that the latent period of this transformation can provide a window of opportunity to prevent the expansion of epileptogenic networks, formation of an epileptic focus, or other comorbidities associated with epileptic activity.

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Publication Details

Journal
PLoS Computational Biology
Published
2024-12-03
DOI
https://doi.org/10.1371/journal.pcbi.1012666
Citations
4
Primary Topic
Neuroscience and Neuropharmacology Research
Type
article
Field-Weighted Citation Impact
1.07

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article

Expansion of epileptogenic networks via neuroplasticity in neural mass models

Pascal Benquet, Elif Köksal Ersöz, Fabrice Wendling
4 citations
PLoS Computational Biology
Neuroscience and Neuropharmacology Research
1.07
article

Expansion of epileptogenic networks via neuroplasticity in neural mass models

Pascal Benquet, Elif Köksal Ersöz, Fabrice Wendling
article en
4 citations

Abstract

Neuroplasticity refers to functional and structural changes in brain regions in response to healthy and pathological activity. Activity dependent plasticity induced by epileptic activity can involve healthy brain regions into the epileptogenic network by perturbing their excitation/inhibition balance. In this article, we present a new neural mass model, which accounts for neuroplasticity, for investigating the possible mechanisms underlying the epileptogenic network expansion. Our multiple-timescale model is inspired by physiological calcium-mediated synaptic plasticity and pathological extrasynaptic N-methyl-D-aspartate (NMDA) dependent plasticity dynamics. The model highlights that synaptic plasticity at excitatory connections and structural changes in the inhibitory system can transform a healthy region into a secondary epileptic focus under recurrent seizures and interictal activity occurring in the primary focus. Our results suggest that the latent period of this transformation can provide a window of opportunity to prevent the expansion of epileptogenic networks, formation of an epileptic focus, or other comorbidities associated with epileptic activity.

PLoS Computational BiologyVol. 20(12)
Inserm (FR), Laboratoire Traitement du Signal et de l'Image (FR), Université de Rennes (FR)
European Commission, HORIZON EUROPE European Research Council
Good health and well-being
Openalex Percentile: Top 23%
Neuroscience and Neuropharmacology Research
1.07
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Expansion of epileptogenic networks via neuroplasticity in neural mass models — Pascal Benquet, Elif Köksal Ersöz, et al. · PLoS Computational Biology (2024) | TGRS Research Map | TGRS