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000155437 0247_ $$2doi$$a10.1186/s13041-021-00809-3
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000155437 037__ $$aDZNE-2021-00643
000155437 041__ $$aEnglish
000155437 082__ $$a610
000155437 1001_ $$aVyas, Yukti$$b0
000155437 245__ $$aIn vitro zinc supplementation alters synaptic deficits caused by autism spectrum disorder-associated Shank2 point mutations in hippocampal neurons.
000155437 260__ $$aLondon$$bBioMed Central$$c2021
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000155437 520__ $$aAutism Spectrum Disorders (ASDs) are neurodevelopmental disorders characterised by deficits in social interactions and repetitive behaviours. ASDs have a strong genetic basis with mutations involved in the development and function of neural circuitry. Shank proteins act as master regulators of excitatory glutamatergic synapses, and Shank mutations have been identified in people with ASD. Here, we have investigated the impact of ASD-associated Shank2 single nucleotide variants (SNVs) at the synaptic level, and the potential of in vitro zinc supplementation to prevent synaptic deficits. Dissociated rat hippocampal cultures expressing enhanced green fluorescent protein (EGFP) tagged Shank2-Wildtype (WT), and ASD-associated Shank2 single nucleotide variants (SNVs: S557N, V717F, and L1722P), were cultured in the absence or presence of 10 μM zinc. In comparison to Shank2-WT, ASD-associated Shank2 SNVs induced significant decreases in synaptic density and reduced the frequency of miniature excitatory postsynaptic currents. These structural and functional ASD-associated synaptic deficits were prevented by chronic zinc supplementation and further support zinc supplementation as a therapeutic target in ASD.
000155437 536__ $$0G:(DE-HGF)POF4-351$$a351 - Brain Function (POF4-351)$$cPOF4-351$$fPOF IV$$x0
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000155437 650_7 $$2Other$$aAutism
000155437 650_7 $$2Other$$aGlutamatergic synapses
000155437 650_7 $$2Other$$aShank2
000155437 650_7 $$2Other$$aZinc supplementation
000155437 650_2 $$2MeSH$$aAnimals
000155437 650_2 $$2MeSH$$aAnimals, Newborn
000155437 650_2 $$2MeSH$$aAutism Spectrum Disorder: genetics
000155437 650_2 $$2MeSH$$aAutism Spectrum Disorder: pathology
000155437 650_2 $$2MeSH$$aDietary Supplements
000155437 650_2 $$2MeSH$$aFemale
000155437 650_2 $$2MeSH$$aGlutamic Acid: metabolism
000155437 650_2 $$2MeSH$$aHippocampus: pathology
000155437 650_2 $$2MeSH$$aMale
000155437 650_2 $$2MeSH$$aNerve Tissue Proteins: genetics
000155437 650_2 $$2MeSH$$aNeurons: drug effects
000155437 650_2 $$2MeSH$$aNeurons: metabolism
000155437 650_2 $$2MeSH$$aNeurons: pathology
000155437 650_2 $$2MeSH$$aPoint Mutation: genetics
000155437 650_2 $$2MeSH$$aRats
000155437 650_2 $$2MeSH$$aSynapses: drug effects
000155437 650_2 $$2MeSH$$aSynapses: pathology
000155437 650_2 $$2MeSH$$aZinc: pharmacology
000155437 7001_ $$aJung, Yewon$$b1
000155437 7001_ $$aLee, Kevin$$b2
000155437 7001_ $$0P:(DE-2719)2810922$$aGarner, Craig C$$b3$$udzne
000155437 7001_ $$0P:(DE-HGF)0$$aMontgomery, Johanna M$$b4
000155437 773__ $$0PERI:(DE-600)2436057-0$$a10.1186/s13041-021-00809-3$$gVol. 14, no. 1, p. 95$$n1$$p95$$tMolecular brain$$v14$$x1756-6606$$y2021
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