Epileptogenesis due to glia-mediated synaptic scaling

Cristina Savin, Jochen Triesch, Michael Meyer-Hermann

Research output: Contribution to journalArticlepeer-review


Homeostatic regulation of neuronal activity is fundamental for the stable functioning of the cerebral cortex. One form of homeostatic synaptic scaling has been recently shown to be mediated by glial cells that interact with neurons through the diffusible messenger tumour necrosis factor-α (TNF-α). Interestingly, TNF-α is also used by the immune system as a proinflammatory messenger, suggesting potential interactions between immune system signalling and the homeostatic regulation of neuronal activity. We present the first computational model of neuron-glia interaction in TNF-α-mediated synaptic scaling. The model shows how under normal conditions the homeostatic mechanism is effective in balancing network activity. After chronic immune activation or TNF-α overexpression by glia, however, the network develops seizure-like activity patterns. This may explain why under certain conditions brain inflammation increases the risk of seizures. Additionally, the model shows that TNF-α diffusion may be responsible for epileptogenesis after localized brain lesions.

Original languageEnglish (US)
Pages (from-to)655-668
Number of pages14
JournalJournal of the Royal Society Interface
Issue number37
StatePublished - Aug 6 2009


  • Epilepsy
  • Homeostasis
  • Neuro-immune interaction
  • Neuron-glia interaction
  • Synaptic scaling

ASJC Scopus subject areas

  • Biotechnology
  • Biophysics
  • Bioengineering
  • Biomaterials
  • Biochemistry
  • Biomedical Engineering


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