ReviewBrain research bulletin2014
Channelopathies and dendritic dysfunction in fragile X syndrome.
Review in Brain research bulletin, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 65 citations in OpenAlex.
- Fmr1 knockout disrupts multiple intrinsic properties via reduced HCN channel activity in mediodorsal thalamocortical neurons.Experimental physiology · 2026Article
- Dysfunctional neural dynamics associated with sensory phenotypes in Fragile X syndrome: insights from mouse models.Journal of neurodevelopmental disorders · 2025Review
- Review
- An integrated transcriptomic and proteomic map of the mouse hippocampus at synaptic resolution.Nature communications · 2025Article
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
- Review
- Physical and functional convergence of the autism risk genes Scn2a and Ank2 in neocortical pyramidal cell dendrites.Neuron · 2024Article
- Characterization of Fragile X Mental Retardation Protein expression in human nociceptors and their axonal projections to the spinal dorsal horn.The Journal of comparative neurology · 2023Article
- Impaired dendritic spike generation in the Fragile X prefrontal cortex is due to loss of dendritic sodium channels.The Journal of physiology · 2023Article
- Unraveling the mysteries of dendritic spine dynamics: Five key principles shaping memory and cognition.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2023Article
- 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
- Active Dendrites and Local Field Potentials: Biophysical Mechanisms and Computational Explorations.Neuroscience · 2022Review
- Ionic Channels as Potential Targets for the Treatment of Autism Spectrum Disorder: A Review.Current neuropharmacology · 2022Review
- Dendrites of Neocortical Pyramidal Neurons: The Key to Understand Intellectual Disability.Cellular and molecular neurobiology · 2022Article
- Channelopathies in fragile X syndrome.Nature reviews. Neuroscience · 2021Review
- Dendritic Integration Dysfunction in Neurodevelopmental Disorders.Developmental neuroscience · 2021Review
- SK2 channel regulation of neuronal excitability, synaptic transmission, and brain rhythmic activity in health and diseases.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Fragile X Mental Retardation Protein Bidirectionally Controls Dendritic IThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Altered dendritic spine function and integration in a mouse model of fragile X syndrome.Nature communications · 2019Article
- Degeneracy in hippocampal physiology and plasticity.Hippocampus · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Dendritic spine abnormalities and the metabotropic glutamate receptor theory put the focus squarely on synapses and protein synthesis as the cellular locus of fragile X syndrome. Synapses however, are only partly responsible for information processing in neuronal networks. Neurotransmitter triggered excitatory postsynaptic potentials (EPSPs) are shaped and integrated by dendritic voltage-gated ion channels. These EPSPs, and in some cases the resultant dendritic spikes, are further modified by dendritic voltage-gated ion channels as they propagate to the soma. If the resultant somatic depolarization is large enough, action potential(s) will be triggered and propagate both orthodromically down the axon, where it may trigger neurotransmitter release, and antidromically back into the dendritic tree, where it can activate and modify dendritic voltage-gated and receptor activated ion channels. Several channelopathies, both soma-dendritic (L-type calcium channels, Slack potassium channels, h-channels, A-type potassium channels) and axo-somatic (BK channels and delayed rectifier potassium channels) were identified in the fmr1-/y mouse model of fragile X syndrome. Pathological function of these channels will strongly influence the excitability of individual neurons as well as overall network function. In this chapter we discuss the role of voltage-gated ion channels in neuronal processing and describe how identified channelopathies in models of fragile X syndrome may play a role in dendritic pathophysiology.
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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.