ArticleProceedings of the National Academy of Sciences of the United States of America2015
Rescue of homeostatic regulation of striatal excitability and locomotor activity in a mouse model of Huntington's disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Therapeutic role of voltage-gated potassium channels in age-related neurodegenerative diseases.Frontiers in cellular neuroscience · 2024Review
- Developmental pyrethroid exposure causes a neurodevelopmental disorder phenotype in mice.PNAS nexus · 2023Article
- Neuron populations use variable combinations of short-term feedback mechanisms to stabilize firing rate.PLoS biology · 2023Article
- Homeostatic plasticity and excitation-inhibition balance: The good, the bad, and the ugly.Current opinion in neurobiology · 2022Review
- Modelling the Human Blood-Brain Barrier in Huntington Disease.International journal of molecular sciences · 2022Article
- Article
- Human amyotrophic lateral sclerosis excitability phenotype screen: Target discovery and validation.Cell reports · 2021Article
- Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021Review
- KCNQ3 is the principal target of retigabine in CA1 and subicular excitatory neurons.Journal of neurophysiology · 2021Article
- Differential Dorsolateral Prefrontal Cortex Proteomic Profiles of Suicide Victims with Mood Disorders.Genes · 2020Article
- The Role of Kv7.2 in Neurodevelopment: Insights and Gaps in Our Understanding.Frontiers in physiology · 2020Review
- Treatment of myotonia congenita with retigabine in mice.Experimental neurology · 2019Article
- Homeostatic synaptic plasticity as a metaplasticity mechanism - a molecular and cellular perspective.Current opinion in neurobiology · 2019Review
- Kv7 channels are upregulated during striatal neuron development and promote maturation of human iPSC-derived neurons.Pflugers Archiv : European journal of physiology · 2018Article
- Potassium channel dysfunction in neurons and astrocytes in Huntington's disease.CNS neuroscience & therapeutics · 2018Review
- Progressive Cl- channel defects reveal disrupted skeletal muscle maturation in R6/2 Huntington's mice.The Journal of general physiology · 2017Article
- Striatal Network Models of Huntington's Disease Dysfunction Phenotypes.Frontiers in computational neuroscience · 2017Article
- The anticonvulsant retigabine suppresses neuronal KScientific reports · 2016Article
- KCNQ channel openers reverse depressive symptoms via an active resilience mechanism.Nature communications · 2016Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
We describe a fast activity-dependent homeostatic regulation of intrinsic excitability of identified neurons in mouse dorsal striatum, the striatal output neurons. It can be induced by brief bursts of activity, is expressed on a time scale of seconds, limits repetitive firing, and can convert regular firing patterns to irregular ones. We show it is due to progressive recruitment of the KCNQ2/3 channels that generate the M current. This homeostatic mechanism is significantly reduced in striatal output neurons of the R6/2 transgenic mouse model of Huntington's disease, at an age when the neurons are hyperactive in vivo and the mice begin to exhibit locomotor impairment. Furthermore, it can be rescued by bath perfusion with retigabine, a KCNQ channel activator, and chronic treatment improves locomotor performance. Thus, M-current dysfunction may contribute to the hyperactivity and network dysregulation characteristic of this neurodegenerative disease, and KCNQ2/3 channel regulation may be a target for therapeutic intervention.
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