ArticleeLife2019
Mutant huntingtin enhances activation of dendritic Kv4 K
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Microglial sTREM2 limits dyskinesia and acts on TrkB to support circuit plasticity.bioRxiv : the preprint server for biology · 2026Article
- Modulation of ion channels as emerging therapeutic targets in the treatment of diabetic neuropathy.EXCLI journal · 2026Review
- State-dependent modulation of spiny projection neurons controls levodopa-induced dyskinesia in a mouse model of Parkinson's disease.Science advances · 2025Article
- Article
- State-dependent modulation of spiny projection neurons controls levodopa-induced dyskinesia in a mouse model of Parkinson's disease.bioRxiv : the preprint server for biology · 2025Article
- GABAergic regulation of striatal spiny projection neurons depends upon their activity state.PLoS biology · 2024Article
- Pathway-specific alterations in striatal excitability and cholinergic modulation in a SAPAP3 mouse model of compulsive motor behavior.Cell reports · 2023Article
- Cell and circuit complexity of the external globus pallidus.Nature neuroscience · 2023Review
- Cholinergic deficits selectively boost cortical intratelencephalic control of striatum in male Huntington's disease model mice.Nature communications · 2023Article
- Acute and protracted abstinence from methamphetamine bidirectionally changes intrinsic excitability of indirect pathway spiny projection neurons in the dorsomedial striatum.Scientific reports · 2022Article
- Potential disease-modifying therapies for Huntington's disease: lessons learned and future opportunities.The Lancet. Neurology · 2022Review
- Activation of histamine type 2 receptors enhances intrinsic excitability of medium spiny neurons in the nucleus accumbens.The Journal of physiology · 2022Article
- Dysregulation of the Basal Ganglia Indirect Pathway in Early SymptomaticThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Neuronal population models reveal specific linear conductance controllers sufficient to rescue preclinical disease phenotypes.iScience · 2021Article
- CalDAG-GEFI mediates striatal cholinergic modulation of dendritic excitability, synaptic plasticity and psychomotor behaviors.Neurobiology of disease · 2021Article
- Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021Review
- Uncoupling the Excitatory Amino Acid Transporter 2 From Its C-Terminal Interactome Restores Synaptic Glutamate Clearance at Corticostriatal Synapses and Alleviates Mutant Huntingtin-Induced Hypokinesia.Frontiers in cellular neuroscience · 2021Article
- SUMOylation of the Kv4.2 Ternary Complex Increases Surface Expression and Current Amplitude by Reducing Internalization in HEK 293 Cells.Frontiers in molecular neuroscience · 2021Article
- Light-regulated voltage-gated potassium channels for acute interrogation of channel function in neurons and behavior.PloS one · 2021Article
- Striatal Kir2 K+ channel inhibition mediates the antidyskinetic effects of amantadine.The Journal of clinical investigation · 2020Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Huntington's disease (HD) is initially characterized by an inability to suppress unwanted movements, a deficit attributable to impaired synaptic activation of striatal indirect pathway spiny projection neurons (iSPNs). To better understand the mechanisms underlying this deficit, striatal neurons in ex vivo brain slices from mouse genetic models of HD were studied using electrophysiological, optical and biochemical approaches. Distal dendrites of iSPNs from symptomatic HD mice were hypoexcitable, a change that was attributable to increased association of dendritic Kv4 potassium channels with auxiliary KChIP subunits. This association was negatively modulated by TrkB receptor signaling. Dendritic excitability of HD iSPNs was rescued by knocking-down expression of Kv4 channels, by disrupting KChIP binding, by restoring TrkB receptor signaling or by lowering mutant-Htt (mHtt) levels with a zinc finger protein. Collectively, these studies demonstrate that mHtt induces reversible alterations in the dendritic excitability of iSPNs that could contribute to the motor symptoms of HD.
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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.