Nov 1, 2018

Homeostatic Inhibitory Control of Cortical Hyperexcitability in Fragile X Syndrome

BioRxiv : the Preprint Server for Biology
Christian A Cea-Del RioMolly M Huntsman


In mouse models of Fragile X Syndrome (FXS), cellular and circuit hyperexcitability are a consequence of altered brain development [reviewed in (Contractor et al., 2015)]. Mechanisms that favor or hinder plasticity of synapses could affect neuronal excitability. This includes inhibitory long term depression (I-LTD): a heterosynaptic form of plasticity that requires the activation of metabotropic glutamate receptors (mGluRs). Differential circuit maturation leads to shifted time points for critical periods of synaptic plasticity across multiple brain regions (Harlow et al., 2010; He et al., 2014), and disruptions of the development of excitatory and inhibitory synaptic function are also observed both during development and into adulthood (Vislay et al., 2013). However, little is known about how this hyperexcitable environment affects inhibitory synaptic plasticity. Our results demonstrate that the somatosensory cortex of the Fmr1 KO mouse model of FXS exhibits increased GABAergic spontaneous activity, a faulty mGluR-mediated inhibitory input and impaired plasticity processes. We find the overall diminished mGluR activation in the Fmr1 KO mice leads to both a decreased spontaneous inhibitory postsynaptic input to principal cells ...Continue Reading

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Mentioned in this Paper

Fragile X Syndrome
Long Term Depression
Receptors, Metabotropic Glutamate
Synaptic Transmission
Biologic Development
Neuronal Plasticity
Leukotrienes D
Structure of Cortex of Kidney

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