Seizure-induced neuronal death is suppressed in the absence of the endogenous lectin galectin-1

Bischoff, V., Deogracias, R., Poirier, F. and Barde, Yves-Alain ORCID: https://orcid.org/0000-0002-7627-461X 2012. Seizure-induced neuronal death is suppressed in the absence of the endogenous lectin galectin-1. Journal of Neuroscience 32 (44) , pp. 15590-15600. 10.1523/JNEUROSCI.4983-11.2012

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Abstract

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.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Subjects:	Q Science > QH Natural history > QH301 Biology
Additional Information:	Pdf uploaded in accordance with publisher's policy at http://www.jneurosci.org/site/misc/ifa_policies.xhtml#copyright (accessed 27/02/2014).
Publisher:	Society for Neuroscience
ISSN:	0270-6474
Date of First Compliant Deposit:	30 March 2016
Last Modified:	13 May 2023 12:26
URI:	https://orca.cardiff.ac.uk/id/eprint/51115

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