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Seizure-induced neuronal death is suppressed in the absence of the endogenous lectin Galectin1

Research output: Contribution to journalArticle

Vincent Bischoff, Ruben Deogracias Pastor, Francoise Poirier, Yves-Alain Barde

Original languageEnglish
Pages (from-to)15590-15600
JournalThe Journal of neuroscience : the official journal of the Society for Neuroscience
Issue number44
Publication statusPublished - Oct 2012

King's Authors


Pilocarpine injection induces epileptic seizures in rodents, an experimental paradigm extensively used to model temporal lobe epilepsy in humans. It includes conspicuous neuronal death in the forebrain and previous work has demonstrated an involvement of the neurotrophin receptor p75NTR in this process. Following the identification of Galectin-1 (Gal-1) as a downstream effector of p75NTR, we examine here the role of this endogenous lectin in pilocarpine-induced cell death in adult mice. We found that most somatostatin-positive neurons also express Gal-1 and that in mice lacking the corresponding gene Lgals1, pilocarpine-induced neuronal death was essentially abolished in the forebrain. We also found that the related lectin Galectin-3 (Gal-3) was strongly upregulated by pilocarpine in microglial cells. This upregulation was absent in Lgals1 mutants and our results with Lgals3-null animals show that Gal-3 is not required for neuronal death in the hippocampus. These findings provide new insights into the roles and regulation of endogenous lectins in the adult CNS and a surprisingly selective proapoptotic role of Gal-1 for a subpopulation of GABAergic interneurons.

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