ArticleHuman molecular genetics2009
Cognitive impairment in Gdi1-deficient mice is associated with altered synaptic vesicle pools and short-term synaptic plasticity, and can be corrected by appropriate learning training.
Article in Human molecular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 58 citations in OpenAlex.
- Dissecting Alzheimer's proteomic landscape through NULISA profiling of brain cell-specific extracellular vesicles.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Impaired Aggrephagy, Interrupted Vesicular Trafficking, and Cellular Stress, Lead to Protein Aggregation, and Synaptic Dysfunction in Cerebellum of Children and Adults with Idiopathic Autism.Cerebellum (London, England) · 2025Article
- Article
- Early-life stress and ovarian hormones alter transcriptional regulation in the nucleus accumbens resulting in sex-specific responses to cocaine.Cell reports · 2023Article
- Astrocytes in human central nervous system diseases: a frontier for new therapies.Signal transduction and targeted therapy · 2023Review
- Damaged mitochondria coincide with presynaptic vesicle loss and abnormalities in alzheimer's disease brain.Acta neuropathologica communications · 2023Article
- Genetic Testing for Malformations of Cortical Development: A Clinical Diagnostic Study.Neurology. Genetics · 2022Article
- Neuronal Cytoskeleton in Intellectual Disability: From Systems Biology and Modeling to Therapeutic Opportunities.International journal of molecular sciences · 2021Review
- Inhibiting glycolysis rescues memory impairment in an intellectual disability Gdi1-null mouse.Metabolism: clinical and experimental · 2021Article
- Timing behavior in genetic murine models of neurological and psychiatric diseases.Experimental brain research · 2021Review
- Intellectual disability and epilepsy due to the K/L-mediated Xq28 duplication: Further evidence of a distinct, dosage-dependent phenotype.American journal of medical genetics. Part A · 2018Article
- Astroglial vesicular network: evolutionary trends, physiology and pathophysiology.Acta physiologica (Oxford, England) · 2018Review
- Impaired αGDI Function in the X-Linked Intellectual Disability: The Impact on Astroglia Vesicle Dynamics.Molecular neurobiology · 2017Article
- Altered fronto-striatal functions in the Gdi1-null mouse model of X-linked Intellectual Disability.Neuroscience · 2017Article
- The intellectual disability protein RAB39B selectively regulates GluA2 trafficking to determine synaptic AMPAR composition.Nature communications · 2015Article
- Memory Formation Shaped by Astroglia.Frontiers in integrative neuroscience · 2015Review
- Intellectual disability and autism spectrum disorders: causal genes and molecular mechanisms.Neuroscience and biobehavioral reviews · 2014Review
- Dynamin1 concentration in the prefrontal cortex is associated with cognitive impairment in Lewy body dementia.F1000Research · 2014Article
- Reduced gamma oscillations in a mouse model of intellectual disability: a role for impaired repetitive neurotransmission?PloS one · 2014Article
- Emerging major synaptic signaling pathways involved in intellectual disability.Molecular psychiatry · 2012Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
The GDI1 gene, responsible in human for X-linked non-specific mental retardation, encodes alphaGDI, a regulatory protein common to all GTPases of the Rab family. Its alteration, leading to membrane accumulation of different Rab GTPases, may affect multiple steps in neuronal intracellular traffic. Using electron microscopy and electrophysiology, we now report that lack of alphaGDI impairs several steps in synaptic vesicle (SV) biogenesis and recycling in the hippocampus. Alteration of the SV reserve pool (RP) and a 50% reduction in the total number of SV in adult synapses may be dependent on a defective endosomal-dependent recycling and may lead to the observed alterations in short-term plasticity. As predicted by the synaptic characteristics of the mutant mice, the short-term memory deficit, observed when using fear-conditioning protocols with short intervals between trials, disappeared when the Gdi1 mutants were allowed to have longer intervals between sessions. Likewise, previously observed deficits in radial maze learning could be corrected by providing less challenging pre-training. This implies that an intact RP of SVs is necessary for memory processing under challenging conditions in mice. The possibility to correct the learning deficit in mice may have clinical implication for future studies in human.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.