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Disrupted information processing in Fmr1-KO mouse layer 4 barrel cortex (Domanski et al 2019)
Tom Morse - MoldelDB admin
fmr1.zip [843]
"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 is unknown. By systematically studying cellular and synaptic properties of layer 4 neurons combined with cellular and network simulations, we explored how the array of phenotypes in Fmr1-knockout (KO) mice produce circuit pathology during development. We show that many of the cellular and synaptic pathologies in Fmr1-KO mice are antagonistic, mitigating circuit dysfunction, and hence may be compensatory to the primary pathology. Overall, the layer 4 network in the Fmr1-KO exhibits significant alterations in spike output in response to thalamocortical input and distorted sensory encoding. This developmental loss of layer 4 sensory encoding precision would contribute to subsequent developmental alterations in layer 4-to-layer 2/3 connectivity and plasticity observed in Fmr1-KO mice, and circuit dysfunction underlying sensory hypersensitivity."
  • Neocortex U1 L4 stellate GLU cell Show Other
  • Abstract integrate-and-fire leaky neuron Show Other
  • Domanski APF, Booker SA, Wyllie DJA, Isaac JTR, Kind PC (2019) Show Other
tom.morse@yale.edu
Domanski et al 2019
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Revisions: 2
Last Time: 6/10/2020 4:45:10 PM
Reviewer: Tom Morse - MoldelDB admin
Owner: Tom Morse - MoldelDB admin