ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Homeostatic responses fail to correct defective amygdala inhibitory circuit maturation in fragile X syndrome.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- When can neuronal activity-dependent homeostatic plasticity maintain circuit-level properties?Journal of computational neuroscience · 2026Article
- Olfactory dysfunction and altered cortical excitability in the mouse model of Fragile X Syndrome.Biological research · 2025Article
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
- Hyperexcitability in the Olfactory Bulb and Impaired Fine Odor Discrimination in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Axonal and presynaptic FMRP: Localization, signal, and functional implications.Hearing research · 2023Review
- Developmental Inhibitory Changes in the Primary Somatosensory Cortex of the Stargazer Mouse Model of Absence Epilepsy.Biomolecules · 2023Article
- Fragile X Syndrome as an interneuronopathy: a lesson for future studies and treatments.Frontiers in neuroscience · 2023Review
- From circuits to behavior: Amygdala dysfunction in fragile X syndrome.Frontiers in integrative neuroscience · 2023Review
- Mechanisms Driving the Emergence of Neuronal Hyperexcitability in Fragile X Syndrome.International journal of molecular sciences · 2022Review
- Dysregulation of GABAA Receptor-Mediated Neurotransmission during the Auditory Cortex Critical Period in the Fragile X Syndrome Mouse Model.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- ER stress-induced modulation of neural activity and seizure susceptibility is impaired in a fragile X syndrome mouse model.Neurobiology of disease · 2021Article
- Channelopathies in fragile X syndrome.Nature reviews. Neuroscience · 2021Review
- Hyperexcitability and Homeostasis in Fragile X Syndrome.Frontiers in molecular neuroscience · 2021Article
- Hyperexcitability of Sensory Neurons in Fragile X Mouse Model.Frontiers in molecular neuroscience · 2021Article
- Decreased reproducibility and abnormal experience-dependent plasticity of network dynamics in Fragile X circuits.Scientific reports · 2020Article
- Elevated FMR1-mRNA and lowered FMRP - A double-hit mechanism for psychiatric features in men with FMR1 premutations.Translational psychiatry · 2020Article
- Abnormal development of auditory responses in the inferior colliculus of a mouse model of Fragile X Syndrome.Journal of neurophysiology · 2020Article
- Developmental studies in fragile X syndrome.Journal of neurodevelopmental disorders · 2020Review
- Dysregulated Prefrontal Cortex Inhibition in Prepubescent and Adolescent Fragile X Mouse Model.Frontiers in molecular neuroscience · 2020Article
- Cellular and synaptic phenotypes lead to disrupted information processing in Fmr1-KO mouse layer 4 barrel cortex.Nature communications · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Fragile X syndrome (FXS) is a debilitating neurodevelopmental disorder thought to arise from disrupted synaptic communication in several key brain regions, including the amygdala, a central processing center for information with emotional and social relevance. Recent studies reveal defects in both excitatory and inhibitory neurotransmission in mature amygdala circuits in Fmr1(-/y) mutants, the animal model of FXS. However, whether these defects are the result of altered synaptic development or simply faulty mature circuits remains unknown. Using a combination of electrophysiological and genetic approaches, we show the development of both presynaptic and postsynaptic components of inhibitory neurotransmission in the FXS amygdala is dynamically altered during critical stages of neural circuit formation. Surprisingly, we observe that there is a homeostatic correction of defective inhibition, which, despite transiently restoring inhibitory synaptic efficacy to levels at or beyond those of control, ultimately fails to be maintained. Using inhibitory interneuron-specific conditional knock-out and rescue mice, we further reveal that fragile X mental retardation protein function in amygdala inhibitory microcircuits can be segregated into distinct presynaptic and postsynaptic components. Collectively, these studies reveal a previously unrecognized complexity of disrupted neuronal development in FXS and therefore have direct implications for establishing novel temporal and region-specific targeted therapies to ameliorate core amygdala-based behavioral symptoms.
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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.