Excitatory/inhibitory synaptic imbalance leads to hippocampal hyperexcitability in mouse models of tuberous sclerosis. - Wikidata - awgldk - TriplyDB

Excitatory/inhibitory synaptic imbalance leads to hippocampal hyperexcitability in mouse models of tuberous sclerosis.

Excitatory/inhibitory synaptic imbalance leads to hippocampal hyperexcitability in mouse models of tuberous sclerosis.

http://www.wikidata.org/entity/Q30540852

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Autism-associated neuroligin-3 mutations commonly impair striatal circuits to boost repetitive behaviors.Impact of Increased Astrocyte Expression of IL-6, CCL2 or CXCL10 in Transgenic Mice on Hippocampal Synaptic Function Characterizing autism spectrum disorders by key biochemical pathways.Excitatory/Inhibitory Balance and Circuit Homeostasis in Autism Spectrum Disorders The neurology of mTOR Channelopathy pathogenesis in autism spectrum disorders Dendritic spine dysgenesis in autism related disorders Intraneuronal Aβ accumulation induces hippocampal neuron hyperexcitability through A-type K(+) current inhibition mediated by activation of caspases and GSK-3.Astroglial glutamate transporter deficiency increases synaptic excitability and leads to pathological repetitive behaviors in mice Early hyperactivity and precocious maturation of corticostriatal circuits in Shank3B(-/-) mice mTOR and MAPK: from localized translation control to epilepsy Common mechanisms of excitatory and inhibitory imbalance in schizophrenia and autism spectrum disorders Activity-dependent adaptations in inhibitory axons MEF2C regulates cortical inhibitory and excitatory synapses and behaviors relevant to neurodevelopmental disorders.Tricornered Kinase Regulates Synapse Development by Regulating the Levels of Wiskott-Aldrich Syndrome Protein In vivo synaptic transmission and morphology in mouse models of Tuberous sclerosis, Fragile X syndrome, Neurofibromatosis type 1, and Costello syndrome Investigating mechanisms underlying neurodevelopmental phenotypes of autistic and intellectual disability disorders: a perspective.Selective suppression of excessive GluN2C expression rescues early epilepsy in a tuberous sclerosis murine model.Inhibition of microRNA 128 promotes excitability of cultured cortical neuronal networks.Decrease of SYNGAP1 in GABAergic cells impairs inhibitory synapse connectivity, synaptic inhibition and cognitive function.mTORC1 Is a Local, Postsynaptic Voltage Sensor Regulated by Positive and Negative Feedback Pathways.Global transcriptional and translational repression in human-embryonic-stem-cell-derived Rett syndrome neurons.Activation of extracellular regulated kinase and mechanistic target of rapamycin pathway in focal cortical dysplasia.Activation of mGluR2/3 underlies the effects of N-acetylcystein on amygdala-associated autism-like phenotypes in a valproate-induced rat model of autism.In vivo evidence for mTORC2-mediated actin cytoskeleton rearrangement in neurons Semaphorin 5A inhibits synaptogenesis in early postnatal- and adult-born hippocampal dentate granule cells.mTOR signaling in epilepsy: insights from malformations of cortical development Tuberous Sclerosis: A New Frontier in Targeted Treatment of Autism The Stress-Induced Atf3-Gelsolin Cascade Underlies Dendritic Spine Deficits in Neuronal Models of Tuberous Sclerosis Complex.REDD2-mediated inhibition of mTOR promotes dendrite retraction induced by axonal injury Elevated CaMKIIα and Hyperphosphorylation of Homer Mediate Circuit Dysfunction in a Fragile X Syndrome Mouse Model.Translational control in synaptic plasticity and cognitive dysfunction Analysis of Proteins That Rapidly Change Upon Mechanistic/Mammalian Target of Rapamycin Complex 1 (mTORC1) Repression Identifies Parkinson Protein 7 (PARK7) as a Novel Protein Aberrantly Expressed in Tuberous Sclerosis Complex (TSC)Advances and Future Directions for Tuberous Sclerosis Complex Research: Recommendations From the 2015 Strategic Planning Conference.An AKT3-FOXG1-reelin network underlies defective migration in human focal malformations of cortical development Hepatocyte Growth Factor Modulates MET Receptor Tyrosine Kinase and β-Catenin Functional Interactions to Enhance Synapse Formation.Neuronal autophagy and neurodevelopmental disorders.A novel Hap1-Tsc1 interaction regulates neuronal mTORC1 signaling and morphogenesis in the brain.mTOR, a Potential Target to Treat Autism Spectrum Disorder.The role of ionotropic glutamate receptors in childhood neurodevelopmental disorders: autism spectrum disorders and fragile x syndrome.

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P2860

Excitatory/inhibitory synaptic imbalance leads to hippocampal hyperexcitability in mouse models of tuberous sclerosis.

http://www.wikidata.org/entity/Q30540852

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Excitatory/inhibitory synaptic ...... models of tuberous sclerosis.

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Excitatory/inhibitory synaptic ...... models of tuberous sclerosis.

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J.NEURON.2013.03.017

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Excitatory/inhibitory synaptic ...... models of tuberous sclerosis.

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Bernardo L Sabatini

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Caroline A Johnson

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Cassandra L Denefrio

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Helen S Bateup

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Jessica L Saulnier

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Karl Kornacker

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P2860

The Role of Epilepsy and Epileptiform EEGs in Autism Spectrum Disorders

Autism and Asperger syndrome: coexistence with other clinical disorders

The Autistic Neuron: Troubled Translation?

Suppression of PKR promotes network excitability and enhanced cognition by interferon-γ-mediated disinhibition

mTOR signaling in growth control and disease

Reversal of learning deficits in a Tsc2+/- mouse model of tuberous sclerosis

A mouse model of TSC1 reveals sex-dependent lethality from liver hemangiomas, and up-regulation of p70S6 kinase activity in Tsc1 null cells

Activity-dependent scaling of quantal amplitude in neocortical neurons

A mouse model of tuberous sclerosis: neuronal loss of Tsc1 causes dysplastic and ectopic neurons, reduced myelination, seizure activity, and limited survival

Regulation of neuronal morphology and function by the tumor suppressors Tsc1 and Tsc2

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