| First Author | Bianchi V | Year | 2012 |
| Journal | PLoS One | Volume | 7 |
| Issue | 1 | Pages | e29763 |
| PubMed ID | 22291894 | Mgi Jnum | J:224063 |
| Mgi Id | MGI:5661150 | Doi | 10.1371/journal.pone.0029763 |
| Citation | Bianchi V, et al. (2012) Forebrain deletion of alphaGDI in adult mice worsens the pre-synaptic deficit at cortico-lateral amygdala synaptic connections. PLoS One 7(1):e29763 |
| abstractText | The GDI1 gene encodes alphaGDI, 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 alphaGDI via specific RAB GTPases acting specifically in forebrain regions at the pre-synaptic sites involved in memory formation. |
