Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Aleksander P. F. Domanski"'
Autor:
Sam A. Booker, Aleksander P. F. Domanski, Owen R. Dando, Adam D. Jackson, John T. R. Isaac, Giles E. Hardingham, David J. A. Wyllie, Peter C. Kind
Publikováno v:
Nature Communications, Vol 10, Iss 1, Pp 1-14 (2019)
Fragile X syndrome and autism spectrum disorders are associated with circuit hyperexcitability, however, its cellular and synaptic bases are not well understood. Here, the authors report abnormal synaptogenesis with an increased prevalence of polysyn
Externí odkaz:
https://doaj.org/article/2fbc40b23b8f4722ab1014116cebc102
Autor:
Aleksander P. F. Domanski, Sam A. Booker, David J. A. Wyllie, John T. R. Isaac, Peter C. Kind
Publikováno v:
Nature Communications, Vol 10, Iss 1, Pp 1-18 (2019)
Somatosensory hypersensitivity in Fmr-1 knockout mice is thought to arise from an increase in cortical circuit excitability. Here, the authors report that the loss of precision of sensory encoding in the Layer 4 of barrel cortex is the primary develo
Externí odkaz:
https://doaj.org/article/ba220841587e4c75bd2141b3e2677e5b
Autor:
Peter C. Kind, Sam A. Booker, Giles E. Hardingham, John T.R. Isaac, Aleksander P. F. Domanski, Owen Dando, David J. A. Wyllie, Adam D. Jackson
Publikováno v:
Nature Communications, Vol 10, Iss 1, Pp 1-14 (2019)
Booker, S A, Domanski, A P F, Dando, O R, Jackson, A D, Isaac, J T R, Hardingham, G E, Wyllie, D J A & Kind, P C 2019, ' Altered dendritic spine function and integration in a mouse model of fragile X syndrome ', Nature Communications, vol. 10, 4813 (2019) . https://doi.org/10.1038/s41467-019-11891-6
Booker, S A, Domanski, A P F, Dando, O R, Jackson, A D, Isaac, J T R, Hardingham, G E, Wyllie, D J A & Kind, P C 2019, ' Altered dendritic spine function and integration in a mouse model of fragile X syndrome ', Nature Communications, vol. 10, 4813 . https://doi.org/10.1038/s41467-019-11891-6
Nature Communications
Booker, S A, Domanski, A P F, Dando, O R, Jackson, A D, Isaac, J T R, Hardingham, G E, Wyllie, D J A & Kind, P C 2019, ' Altered dendritic spine function and integration in a mouse model of fragile X syndrome ', Nature Communications, vol. 10, 4813 (2019) . https://doi.org/10.1038/s41467-019-11891-6
Booker, S A, Domanski, A P F, Dando, O R, Jackson, A D, Isaac, J T R, Hardingham, G E, Wyllie, D J A & Kind, P C 2019, ' Altered dendritic spine function and integration in a mouse model of fragile X syndrome ', Nature Communications, vol. 10, 4813 . https://doi.org/10.1038/s41467-019-11891-6
Nature Communications
Cellular and circuit hyperexcitability are core features of fragile X syndrome and related autism spectrum disorder models. However, the cellular and synaptic bases of this hyperexcitability have proved elusive. We report in a mouse model of fragile
Publikováno v:
Nature Communications, Vol 10, Iss 1, Pp 1-18 (2019)
Domanski, A P F, Booker, S A, Wyllie, D J A, Isaac, J T R & Kind, P C 2019, ' Cellular and synaptic phenotypes lead to disrupted information processing in Fmr1-KO mouse layer 4 barrel cortex ', Nature Communications, vol. 10, 4814 . https://doi.org/10.1038/s41467-019-12736-y
Domanski, A P F, Booker, S A, Wyllie, D J A, Isaac, J T R & Kind, P C 2019, ' Cellular and synaptic phenotypes lead to disrupted information processing in Fmr1-KO mouse layer 4 barrel cortex ', Nature Communications, vol. 10, 4814 (2019) . https://doi.org/10.1038/s41467-019-12736-y
Nature Communications
Domanski, A P F, Booker, S A, Wyllie, D J A, Isaac, J T R & Kind, P C 2019, ' Cellular and synaptic phenotypes lead to disrupted information processing in Fmr1-KO mouse layer 4 barrel cortex ', Nature Communications, vol. 10, 4814 . https://doi.org/10.1038/s41467-019-12736-y
Domanski, A P F, Booker, S A, Wyllie, D J A, Isaac, J T R & Kind, P C 2019, ' Cellular and synaptic phenotypes lead to disrupted information processing in Fmr1-KO mouse layer 4 barrel cortex ', Nature Communications, vol. 10, 4814 (2019) . https://doi.org/10.1038/s41467-019-12736-y
Nature Communications
Sensory hypersensitivity is a common and debilitating feature of neurodevelopmental disorders such as Fragile X Syndrome (FXS). How developmental changes in neuronal function culminate in network dysfunction that underlies sensory hypersensitivities