ArticleMolecular psychiatry2020
Identification of a molecular locus for normalizing dysregulated GABA release from interneurons in the Fragile X brain.
Article in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 69 citations in OpenAlex.
- Dysfunctional neural dynamics associated with sensory phenotypes in Fragile X syndrome: insights from mouse models.Journal of neurodevelopmental disorders · 2025Review
- Input-Specific Organization of Intrinsic Excitability Expands Coding Capacity of Fast-Spiking Auditory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Conifer metabolite pisiferic acid restores activity in human Kv1.2 potassium channels carrying pathogenic sequence variants.iScience · 2025Article
- Neuronal potassium channel activity triggers initiation of mRNA translation through binding of translation regulators.Science advances · 2025Article
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
- Molecular Profiling of Mouse Models of Loss or Gain of Function of the KCNT1 (Slack) Potassium Channel and Antisense Oligonucleotide Treatment.Biomolecules · 2024Article
- Roles of KCNA2 in Neurological Diseases: from Physiology to Pathology.Molecular neurobiology · 2024Review
- Calcium-Dependent Regulation of Neuronal Excitability Is Rescued in Fragile X Syndrome by a Tat-Conjugated N-Terminal Fragment of FMRP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Oligodendrocyte-derived LGI3 and its receptor ADAM23 organize juxtaparanodal Kv1 channel clustering for short-term synaptic plasticity.Cell reports · 2024Article
- On-Tissue Spatial Proteomics Integrating MALDI-MS Imaging with Shotgun Proteomics Reveals Soy Consumption-Induced Protein Changes in a Fragile X Syndrome Mouse Model.ACS chemical neuroscience · 2024Article
- Cerebellar contribution to autism-relevant behaviors in fragile X syndrome models.Cell reports · 2023Article
- RNA-Binding Proteins: A Role in Neurotoxicity?Neurotoxicity research · 2023Review
- Increased Inhibition May Contribute to Maintaining Normal Network Function in the Ventral Hippocampus of a Fmr1-Targeted Transgenic Rat Model of Fragile X Syndrome.Brain sciences · 2023Article
- Cognitive-Affective Functions of the Cerebellum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Social memory deficit caused by dysregulation of the cerebellar vermis.Nature communications · 2023Article
- Autistic-like behavior and cerebellar dysfunction in Bmal1 mutant mice ameliorated by mTORC1 inhibition.Molecular psychiatry · 2023Article
- Axonal and presynaptic FMRP: Localization, signal, and functional implications.Hearing research · 2023Review
- Fragile X Syndrome as an interneuronopathy: a lesson for future studies and treatments.Frontiers in neuroscience · 2023Review
- Rescue of sharp wave-ripples and prevention of network hyperexcitability in the ventral but not the dorsal hippocampus of a rat model of fragile X syndrome.Frontiers in cellular neuroscience · 2023Article
- Prefrontal circuits guiding social preference: Implications in autism spectrum disorder.Neuroscience and biobehavioral reviews · 2022Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Principal neurons encode information by varying their firing rate and patterns precisely fine-tuned through GABAergic interneurons. Dysregulation of inhibition can lead to neuropsychiatric disorders, yet little is known about the molecular basis underlying inhibitory control. Here, we find that excessive GABA release from basket cells (BCs) attenuates the firing frequency of Purkinje neurons (PNs) in the cerebellum of Fragile X Mental Retardation 1 (Fmr1) knockout (KO) mice, a model of Fragile X Syndrome (FXS) with abrogated expression of the Fragile X Mental Retardation Protein (FMRP). This over-inhibition originates from increased excitability and Ca
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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.