ReviewCells2021
Interneuron Dysfunction and Inhibitory Deficits in Autism and Fragile X Syndrome.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
- Review
- CRISPR-Enabled functional genomics in hPSCs-derived neural models for autism spectrum disorder.Metabolic brain disease · 2026Review
- Hippocampal Astrocytes Impact Postnatal Development of Inhibitory Connections, Parvalbumin Levels, Social, and Spatial Navigation Behaviors in a Mouse Model of Fragile X Syndrome.Journal of neurochemistry · 2026Article
- CRISPR screens in human neural organoids and assembloids.Nature protocols · 2026Review
- Review
- Structural-functional connectivity coupling in motor-brain networks following acute ischemic stroke.Journal of neuroengineering and rehabilitation · 2026Article
- 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
- Psychedelic Modulation of Excitation/Inhibition Balance: A Dual-Phase Neurodevelopmental Model.ACS chemical neuroscience · 2026Review
- FMRP restoration in parvalbumin interneurons: A circuit-specific improvement of visual learning in fragile X syndrome.iScience · 2025Article
- Synaptic Synchronization-Based Learning of Pattern Separation in Self-Organizing Probabilistic Spiking Neural Networks.bioRxiv : the preprint server for biology · 2025Article
- Network Activity Shapes Inhibitory Synaptic Development in the Mouse Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- GABAergic interneurons contribute to the fatal seizure phenotype of CLN2 disease mice.JCI insight · 2025Article
- Exploring the Relationship Between Fragile X Syndrome and Autism: A Bibliometric Analysis of Global Research Trends.Cureus · 2025Review
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
- The NKCC1 Inhibitor Bumetanide Restores Cortical Feedforward Inhibition and Lessens Sensory Hypersensitivity in Early Postnatal Fragile X Mice.Biological psychiatry · 2025Article
- Auditory steady-state response deficits in Fragile X Syndrome implicate deficits in stimulus representation maintenance and GABAergic modulation.medRxiv : the preprint server for health sciences · 2025Article
- Host brain environmental influences on transplanted medial ganglionic eminence progenitors.Scientific reports · 2024Article
- Rare genetic brain disorders with overlapping neurological and psychiatric phenotypes.Nature reviews. Neurology · 2024Review
- The "psychiatric" neuron: the psychic neuron of the cerebral cortex, revisited.Frontiers in human neuroscience · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The alteration of excitatory-inhibitory (E-I) balance has been implicated in various neurological and psychiatric diseases, including autism spectrum disorder (ASD). Fragile X syndrome (FXS) is a single-gene disorder that is the most common known cause of ASD. Understanding the molecular and physiological features of FXS is thought to enhance our knowledge of the pathophysiology of ASD. Accumulated evidence implicates deficits in the inhibitory circuits in FXS that tips E-I balance toward excitation. Deficits in interneurons, the main source of an inhibitory neurotransmitter, gamma-aminobutyric acid (GABA), have been reported in FXS, including a reduced number of cells, reduction in intrinsic cellular excitability, or weaker synaptic connectivity. Manipulating the interneuron activity ameliorated the symptoms in the FXS mouse model, which makes it reasonable to conceptualize FXS as an interneuronopathy. While it is still poorly understood how the developmental profiles of the inhibitory circuit go awry in FXS, recent works have uncovered several developmental alterations in the functional properties of interneurons. Correcting disrupted E-I balance by potentiating the inhibitory circuit by targeting interneurons may have a therapeutic potential in FXS. I will review the recent evidence about the inhibitory alterations and interneuron dysfunction in ASD and FXS and will discuss the future directions of this field.
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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.