ArticleNeuron2013
Excitatory/inhibitory synaptic imbalance leads to hippocampal hyperexcitability in mouse models of tuberous sclerosis.
Article in Neuron, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
224 citing papers in PubMed, 345 citations in OpenAlex.
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- Conditional Modeling of GNAO1 Disorder Dissociates Circuit Specific Contributions to Pathology and Rationalizes Ameliorative Strategies.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Delayed forebrain excitatory and inhibitory neurogenesis in STRADA-related megalencephaly via mTOR hyperactivity.Stem cell reports · 2026Article
- Ploidy and neuron size impact nervous system development and function in Xenopus.Cell reports · 2026Article
- Postnatal reduction of eIF4E overexpression in D1-SPNs ameliorates KCNQ channel dysfunction, hyperexcitability and ASD-like behaviours.Cellular and molecular life sciences : CMLS · 2026Article
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- Anti-seizure potential of J4, an equilibrative nucleoside transporter 1 inhibitor, in a mouse model of tuberous sclerosis complex in response to pentylenetetrazol.Cell & bioscience · 2026Article
- Memory processing in neurodevelopmental disorders: linking behavioral, circuits, and molecular scales.Frontiers in cellular neuroscience · 2026Review
- Impaired nuclear PTEN function drives macrocephaly, lymphadenopathy and late-onset cancer in PTEN hamartoma tumour syndrome.Disease models & mechanisms · 2026Article
- Neuronal hyperactivity becomes mTORC1 independent due to transcriptional changes in tuberous sclerosis complex disease models.Cell reports · 2025Article
- Network Activity Shapes Inhibitory Synaptic Development in the Mouse Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Disentangling metabolic and neurovascular timescales supporting cognitive processes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Division of labor among H3K4 methyltransferases defines distinct facets of homeostatic plasticity.Cell reports · 2025Article
- Terminal nucleotidyltransferaseRNA (New York, N.Y.) · 2025Article
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- Tsc1 deletion in Purkinje neurons disrupts the axon initial segment, impairing excitability and cerebellar function.Neurobiology of disease · 2025Article
164 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Neural circuits are regulated by activity-dependent feedback systems that tightly control network excitability and which are thought to be crucial for proper brain development. Defects in the ability to establish and maintain network homeostasis may be central to the pathogenesis of neurodevelopmental disorders. Here, we examine the function of the tuberous sclerosis complex (TSC)-mTOR signaling pathway, a common target of mutations associated with epilepsy and autism spectrum disorder, in regulating activity-dependent processes in the mouse hippocampus. We find that the TSC-mTOR pathway is a central component of a positive feedback loop that promotes network activity by repressing inhibitory synapses onto excitatory neurons. In Tsc1 KO neurons, weakened inhibition caused by deregulated mTOR alters the balance of excitatory and inhibitory synaptic transmission, leading to hippocampal hyperexcitability. These findings identify the TSC-mTOR pathway as a regulator of neural network activity and have implications for the neurological dysfunction in disorders exhibiting deregulated mTOR signaling.
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What OpenQuestion holds
Registered trials
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.