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Epilepsy: synapses stuck in childhood

Nature Medicine volume 15, pages 1126–1127 (2009)Cite this article

Mouse experiments show how mutation of a gene involved in human epilepsy causes hyperexcitability of the neuronal network (pages 1208–1214). The mutations interfere with the maturation of excitatory synapses during postnatal development.

Mutations in genes that code for ion channels are the main cause of idiopathic epilepsies—that is, epilepsies characterized by no overt structural alterations in the brain1. One exception is leucine-rich, glioma-inactivated gene-1 (LGI1), a nonion channel gene that is implicated in about half the cases of autosomal dominant lateral temporal lobe epilepsy (ADLTE)1,2,3. ADLTE is a rare syndrome whose symptoms usually begin in adolescence. It is characterized by partial seizures originating in the lateral temporal lobe, accompanied by auditory and sometimes even visual hallucinations1,3.

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Figure 1: Effects of LGI1 mutation on circuit development and excitability.

Marina Corral

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  1. Matteo Caleo is at Istituto di Neuroscienze, Consiglio Nazionale delle Ricerche, Pisa, Italy.,

    Matteo Caleo

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Correspondence to Matteo Caleo.

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Caleo, M. Epilepsy: synapses stuck in childhood. Nat Med 15, 1126–1127 (2009). https://doi.org/10.1038/nm1009-1126

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