ArticleMolecular brain2016
Synaptic plasticity and spatial working memory are impaired in the CD mouse model of Williams-Beuren syndrome.
Article in Molecular brain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Brain Monoamine Deficits in the CD Mouse Model of Williams-Beuren Syndrome.Biomolecules · 2025Article
- TAF15 downregulation contributes to the benefits of physical training on dendritic spines and working memory in aged mice.Aging cell · 2024Article
- Genetic mechanisms for impaired synaptic plasticity in schizophrenia revealed by computational modeling.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Loss of spines in the prelimbic cortex is detrimental to working memory in mice with early-life adversity.Molecular psychiatry · 2023Article
- Early Neurobehavioral Characterization of the CD Mouse Model of Williams-Beuren Syndrome.Cells · 2023Article
- Review
- Williams syndrome.Nature reviews. Disease primers · 2021Review
- Gtf2i and Gtf2ird1 mutation do not account for the full phenotypic effect of the Williams syndrome critical region in mouse models.Human molecular genetics · 2019Article
- Expression of the RNA methyltransferase Nsun5 is essential for developing cerebral cortex.Molecular brain · 2019Article
- Metabolic etiologies in West syndrome.Epilepsia open · 2018Review
- Epigallocatechin-3-gallate improves cardiac hypertrophy and short-term memory deficits in a Williams-Beuren syndrome mouse model.PloS one · 2018Article
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Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mice heterozygous for a complete deletion (CD) equivalent to the most common deletion found in individuals with Williams-Beuren syndrome (WBS) recapitulate relevant features of the neurocognitive phenotype, such as hypersociability, along with some neuroanatomical alterations in specific brain areas. However, the pathophysiological mechanisms underlying these phenotypes still remain largely unknown. We have studied the synaptic function and cognition in CD mice using hippocampal slices and a behavioral test sensitive to hippocampal function. We have found that long-term potentiation (LTP) elicited by theta burst stimulation (TBS) was significantly impaired in hippocampal field CA1 of CD animals. This deficit might be associated with the observed alterations in spatial working memory. However, we did not detect changes in presynaptic function, LTP induction mechanisms or AMPA and NMDA receptor function. Reduced levels of Brain-derived neurotrophic factor (BDNF) were present in the CA1-CA3 hippocampal region of CD mice, which could account for LTP deficits in these mice. Taken together, these results suggest a defect of CA1 synapses in CD mice to sustain synaptic strength after stimulation. These data represent the first description of synaptic functional deficits in CD mice and further highlights the utility of the CD model to study the mechanisms underlying the WBS neurocognitive profile.
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