ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Altered neocortical rhythmic activity states in Fmr1 KO mice are due to enhanced mGluR5 signaling and involve changes in excitatory circuitry.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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114 citing papers in PubMed, 173 citations in OpenAlex.
- The mMolecular psychiatry · 2026Article
- Impaired behavioral inhibition in Fmr1 KO mice is linked to disrupted visual cortex theta oscillations.Cell reports · 2026Article
- Contribution of astrocytic calcium signaling to auditory hypersensitivity in a mouse model of fragile X syndrome.Neurobiology of disease · 2026Article
- Enhanced CB1 receptor function in GABAergic neurons mediates hyperexcitability and impaired sensory-driven synchrony of cortical circuits in Fragile X Syndrome model mice.Molecular psychiatry · 2026Article
- Article
- A human electrophysiological signature of Fragile X pathophysiology is shared in V1 of Fmr1Nature communications · 2026Article
- Astrocytic GABA controls fidelity of temporal cortical processing in Fragile X Syndrome.Neurobiology of disease · 2026Article
- Cell-intrinsic mechanisms underlying spontaneous activity in the mouse visual cortical slice: implications for fragile X pathophysiology.Journal of neurophysiology · 2026Article
- Mitochondrial membrane junction-mediated ATP channeling drives activity-dependent glucose metabolism.bioRxiv : the preprint server for biology · 2025Article
- Aberrant hippocampal gamma oscillations in a mouse model of fragile X syndrome: insights from in vitro slice models.Molecular autism · 2025Article
- Cortical layer-specific abnormalities in auditory responses in a mouse model of Fragile X Syndrome.Neurobiology of disease · 2025Article
- Frontal cortex hyperactivation and gamma desynchrony in Fragile X syndrome: Correlates of auditory hypersensitivity.PloS one · 2025Article
- Delayed onset of striatal projection neuron hyperexcitability inFrontiers in cellular neuroscience · 2025Article
- Clinicopathologic Dissociation: Robust Lafora Body Accumulation in Malin KO Mice Without Observable Changes in Home-Cage Behavior.The Journal of comparative neurology · 2024Article
- Hypnotic treatment improves sleep architecture and EEG disruptions and rescues memory deficits in a mouse model of fragile X syndrome.Cell reports · 2024Article
- FOXP1 regulates the development of excitatory synaptic inputs onto striatal neurons and induces phenotypic reversal with reinstatement.Science advances · 2024Article
- Female-specific dysfunction of sensory neocortical circuits in a mouse model of autism mediated by mGluR5 and estrogen receptor α.Cell reports · 2024Article
- Cerebellar contribution to autism-relevant behaviors in fragile X syndrome models.Cell reports · 2023Article
- Article
- Group I metabotropic glutamate receptor-triggered temporally patterned action potential-dependent spontaneous synaptic transmission in mouse MNTB neurons.Hearing research · 2023Article
54 more citing papers are in PubMed but not listed here.
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3 authors at 1 institution in 1 country.
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Abstract
Despite the pronounced neurological deficits associated with mental retardation and autism, the degree to which neocortical circuit function is altered remains unknown. Here, we study changes in neocortical network function in the form of persistent activity states in the mouse model of fragile X syndrome--the Fmr1 knock-out (KO). Persistent activity states, or UP states, in the neocortex underlie the slow oscillation which occurs predominantly during slow-wave sleep, but may also play a role during awake states. We show that spontaneously occurring UP states in the primary somatosensory cortex are 38-67% longer in Fmr1 KO slices. In vivo, UP states reoccur with a clear rhythmic component consistent with that of the slow oscillation and are similarly longer in the Fmr1 KO. Changes in neocortical excitatory circuitry likely play the major role in this alteration as supported by three findings: (1) longer UP states occur in slices of isolated neocortex, (2) pharmacologically isolated excitatory circuits in Fmr1 KO neocortical slices display prolonged bursting states, and (3) selective deletion of Fmr1 in cortical excitatory neurons is sufficient to cause prolonged UP states whereas deletion in inhibitory neurons has no effect. Excess signaling mediated by the group 1 glutamate metabotropic receptor, mGluR5, contributes to the longer UP states. Genetic reduction or pharmacological blockade of mGluR5 rescues the prolonged UP state phenotype. Our results reveal an alteration in network function in a mouse model of intellectual disability and autism which may impact both slow-wave sleep and information processing during waking states.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.