Forced neuronal interactions cause poor communication.

Détails

Ressource 1Télécharger: 5_28265586_Postprint.pdf (4953.42 [Ko])
Etat: Serval
Version: Author's accepted manuscript
ID Serval
serval:BIB_236F7653A30E
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Editorial
Collection
Publications
Titre
Forced neuronal interactions cause poor communication.
Périodique
Neurogenesis (Austin, Tex.)
Auteur(s)
Krzisch M., Toni N.
ISSN-L
2326-2133
Statut éditorial
Publié
Date de publication
2017
Peer-reviewed
Oui
Volume
4
Numéro
1
Pages
e1286424
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish
Résumé
Post-natal hippocampal neurogenesis plays a role in hippocampal function, and neurons born post-natally participate to spatial memory and mood control. However, a great proportion of granule neurons generated in the post-natal hippocampus are eliminated during the first 3 weeks of their maturation, a mechanism that depends on their synaptic integration. In a recent study, we examined the possibility of enhancing the synaptic integration of neurons born post-natally, by specifically overexpressing synaptic cell adhesion molecules in these cells. Synaptic cell adhesion molecules are transmembrane proteins mediating the physical connection between pre- and post-synaptic neurons at the synapse, and their overexpression enhances synapse formation. Accordingly, we found that overexpressing synaptic adhesion molecules increased the synaptic integration and survival of newborn neurons. Surprisingly, the synaptic adhesion molecule with the strongest effect on new neurons' survival, Neuroligin-2A, decreased memory performances in a water maze task. We present here hypotheses explaining these surprising results, in the light of the current knowledge of the mechanisms of synaptic integration of new neurons in the post-natal hippocampus.

Pubmed
Création de la notice
14/03/2017 11:46
Dernière modification de la notice
04/09/2018 7:08
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