http://www.cnr.it/ontology/cnr/individuo/prodotto/ID200453
Forebrain deletion of ?GDI in adult mice worsens the pre-synaptic deficit at cortico-lateral amygdala synaptic connections. (Articolo in rivista)
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- Forebrain deletion of ?GDI in adult mice worsens the pre-synaptic deficit at cortico-lateral amygdala synaptic connections. (Articolo in rivista) (literal)
- Anno
- 2012-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1371/journal.pone.0029763 (literal)
- Alternative label
Bianchi V, Gambino F, Muzio L, Toniolo D, Humeau Y, D'Adamo P. (2012)
Forebrain deletion of ?GDI in adult mice worsens the pre-synaptic deficit at cortico-lateral amygdala synaptic connections.
in PloS one
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Bianchi V, Gambino F, Muzio L, Toniolo D, Humeau Y, D'Adamo P. (literal)
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- http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0029763 (literal)
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- Institut Interdiciplinaire de Neuroscience Centre National de la Recherche Scientifique UMR5297, University of Bordeaux, Bordeaux, France; Division of Genetics and Cell Biology, San Raffaele Scientific Institute, Milan, Italy and Institute of Molecular Genetics-CNR, Pavia, Italy; Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy; Dulbecco Telethon Institute at Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy; Departement des Neurosciences Fondamentales, CMU, Geneve, Suisse; Centre National de la Recherche Scientifique UPR3212, CNRS, University of Strasbourg, Strasbourg, France (literal)
- Titolo
- Forebrain deletion of ?GDI in adult mice worsens the pre-synaptic deficit at cortico-lateral amygdala synaptic connections. (literal)
- Abstract
- The GDI1 gene encodes ?GDI, which retrieves inactive GDP-bound RAB from membranes to form a cytosolic pool awaiting vesicular release. Mutations in GDI1 are responsible for X-linked Intellectual Disability. Characterization of the Gdi1-null mice has revealed alterations in the total number and distribution of hippocampal and cortical synaptic vesicles, hippocampal short-term synaptic plasticity and specific short-term memory deficits in adult mice, which are possibly caused by alterations of different synaptic vesicle recycling pathways controlled by several RAB GTPases. However, interpretation of these studies is complicated by the complete ablation of Gdi1 in all cells in the brain throughout development. In this study, we generated conditionally gene-targeted mice in which the knockout of Gdi1 is restricted to the forebrain, hippocampus, cortex and amygdala and occurs only during postnatal development. Adult mutant mice reproduce the short-term memory deficit previously reported in Gdi1-null mice. Surprisingly, the delayed ablation of Gdi1 worsens the pre-synaptic phenotype at cortico-amygdala synaptic connections compared to Gdi1-null mice. These results suggest a pivotal role of ?GDI via specific RAB GTPases acting specifically in forebrain regions at the pre-synaptic sites involved in memory formation. (literal)
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