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• W4225080779 abstract "Autism Spectrum Disorder (ASD), Rett syndrome (RTT) and Angelman Syndrome (AS) are neurodevelopmental disorders (NDDs) that share several clinical characteristics, including displays of repetitive movements, developmental delays, language deficits, intellectual disability, and increased susceptibility to epilepsy. While several reviews address the biological basis of non-seizure-related ASD phenotypes, here, I highlight some shared biological mechanisms that may contribute to increased seizure susceptibility. I focus on genetic studies identifying the anatomical origin of the seizure phenotype in loss-of-function, monogenic, mouse models of these NDDs, combined with insights gained from complementary studies quantifying levels of synaptic excitation and inhibition. Epilepsy is characterized by a sudden, abnormal increase in synchronous activity within neuronal networks, that is posited to arise from excess excitation, largely driven by reduced synaptic inhibition. Primarily for this reason, elevated network excitability is proposed to underlie the causal basis for the ASD, RTT, and AS phenotypes. Although, mouse models of these disorders replicate aspects of the human condition, i.e., hyperexcitability discharges or seizures on cortical electroencephalograms, measures at the synaptic level often reveal deficits in excitatory synaptic transmission, rather than too much excitation. Resolving this apparent paradox has direct implications regarding expected outcomes of manipulating GABAergic tone. In particular, in NDDs associated with seizures, cortical circuits can display reduced, rather than normal or increased levels of synaptic excitation, and therefore suggested treatments aimed at increasing inhibition could further promote hypoactivity instead of normality. In this review, I highlight shared mechanisms across animal models for ASD, RTT, and AS with reduced synaptic excitation that nevertheless promote hyperexcitability in cortical circuits." @default.
• W4225080779 created "2022-04-30" @default.
• W4225080779 creator A5009763014 @default.
• W4225080779 date "2022-04-29" @default.
• W4225080779 modified "2023-10-02" @default.
• W4225080779 title "Paradoxical Hyperexcitability in Disorders of Neurodevelopment" @default.
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• W4225080779 cites W1559742681 @default.
• W4225080779 cites W1565060794 @default.
• W4225080779 cites W1964437684 @default.
• W4225080779 cites W1970789949 @default.
• W4225080779 cites W1983532821 @default.
• W4225080779 cites W1987055742 @default.
• W4225080779 cites W1987397557 @default.
• W4225080779 cites W1992577657 @default.
• W4225080779 cites W1998336883 @default.
• W4225080779 cites W2006296612 @default.
• W4225080779 cites W2009759904 @default.
• W4225080779 cites W2018882057 @default.
• W4225080779 cites W2020808135 @default.
• W4225080779 cites W2021281924 @default.
• W4225080779 cites W2021996855 @default.
• W4225080779 cites W2026751327 @default.
• W4225080779 cites W2031215168 @default.
• W4225080779 cites W2037910525 @default.
• W4225080779 cites W2038253875 @default.
• W4225080779 cites W2040567458 @default.
• W4225080779 cites W2040574649 @default.
• W4225080779 cites W2041807010 @default.
• W4225080779 cites W2047378045 @default.
• W4225080779 cites W2052721941 @default.
• W4225080779 cites W2061072142 @default.
• W4225080779 cites W2073489133 @default.
• W4225080779 cites W2075059777 @default.
• W4225080779 cites W2077208091 @default.
• W4225080779 cites W2086236510 @default.
• W4225080779 cites W2092597282 @default.
• W4225080779 cites W2104135721 @default.
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• W4225080779 cites W2127311839 @default.
• W4225080779 cites W2127975841 @default.
• W4225080779 cites W2129032286 @default.
• W4225080779 cites W2138688363 @default.
• W4225080779 cites W2155438906 @default.
• W4225080779 cites W2162423225 @default.
• W4225080779 cites W2164163668 @default.
• W4225080779 cites W2178727006 @default.
• W4225080779 cites W2320983896 @default.
• W4225080779 cites W2463052690 @default.
• W4225080779 cites W2471459799 @default.
• W4225080779 cites W2546757431 @default.
• W4225080779 cites W2588392021 @default.
• W4225080779 cites W2604505267 @default.
• W4225080779 cites W2610190082 @default.
• W4225080779 cites W2623777044 @default.
• W4225080779 cites W2742769516 @default.
• W4225080779 cites W2744804789 @default.
• W4225080779 cites W2790548666 @default.
• W4225080779 cites W2797102036 @default.
• W4225080779 cites W2800285111 @default.
• W4225080779 cites W2883065428 @default.
• W4225080779 cites W2883393209 @default.
• W4225080779 cites W2926987093 @default.
• W4225080779 cites W2941525855 @default.
• W4225080779 cites W2950040155 @default.
• W4225080779 cites W2950333680 @default.
• W4225080779 cites W2955503846 @default.
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• W4225080779 cites W3005328263 @default.
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• W4225080779 cites W3040365400 @default.
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• W4225080779 cites W3188831673 @default.
• W4225080779 cites W3192500124 @default.
• W4225080779 cites W3197611578 @default.
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• W4225080779 cites W4238213814 @default.
• W4225080779 cites W4242103952 @default.
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• W4225080779 doi "https://doi.org/10.3389/fnmol.2022.826679" @default.
• W4225080779 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35571370" @default.
• W4225080779 hasPublicationYear "2022" @default.
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