ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
NKCC1 knockdown decreases neuron production through GABA(A)-regulated neural progenitor proliferation and delays dendrite development.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 71 citations in OpenAlex.
- Learning Dynamics in Biophysical Spiking Network Models Are Shaped by KCC2/NKCC1 Cotransporter Stoichiometry.The European journal of neuroscience · 2026Article
- Relationship Between Gut Microbiota and Cancer Neuro-Immunity.Microbial biotechnology · 2026Review
- Maturation of GABAergic signalling times the opening of a critical period in Drosophila melanogaster.Scientific reports · 2025Article
- Cortical regulation of neurogenesis and cell proliferation in the ventral subventricular zone.Cell reports · 2023Article
- Loss of Slc12a2 specifically in pancreatic β-cells drives metabolic syndrome in mice.PloS one · 2022Article
- Loss of KCC2 in GABAergic Neurons Causes Seizures and an Imbalance of Cortical Interneurons.Frontiers in molecular neuroscience · 2022Article
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- How Staying Negative Is Good for the (Adult) Brain: Maintaining Chloride Homeostasis and the GABA-Shift in Neurological Disorders.Frontiers in molecular neuroscience · 2022Review
- Clinical characterization and further confirmation of the autosomal recessive SLC12A2 disease.Journal of human genetics · 2021Article
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- The Contribution of Dysfunctional Chloride Channels to Neurovascular Deficiency and Neurodegeneration.Frontiers in pharmacology · 2021Article
- The Structural E/I Balance Constrains the Early Development of Cortical Network Activity.Frontiers in cellular neuroscience · 2021Article
- SLC12A2 variants cause a neurodevelopmental disorder or cochleovestibular defect.Brain : a journal of neurology · 2020Article
- Article
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- Sevoflurane-Induced Dysregulation of Cation-Chloride Cotransporters NKCC1 and KCC2 in Neonatal Mouse Brain.Molecular neurobiology · 2020Article
- From Neural Tube Formation Through the Differentiation of Spinal Cord Neurons: Ion Channels in Action During Neural Development.Frontiers in molecular neuroscience · 2020Article
- Overlapping migratory mechanisms between neural progenitor cells and brain tumor stem cells.Cellular and molecular life sciences : CMLS · 2019Review
- Kilquist syndrome: A novel syndromic hearing loss disorder caused by homozygous deletion of SLC12A2.Human mutation · 2019Article
- Neural stem cells: origin, heterogeneity and regulation in the adult mammalian brain.Development (Cambridge, England) · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Signaling through GABA(A) receptors controls neural progenitor cell (NPC) development in vitro and is altered in schizophrenic and autistic individuals. However, the in vivo function of GABA(A) signaling on neural stem cell proliferation, and ultimately neurogenesis, remains unknown. To examine GABA(A) function in vivo, we electroporated plasmids encoding short-hairpin (sh) RNA against the Na-K-2Cl cotransporter NKCC1 (shNKCC1) in NPCs of the neonatal subventricular zone in mice to reduce GABA(A)-induced depolarization. Reduced GABA(A) depolarization identified by a loss of GABA(A)-induced calcium responses in most electroporated NPCs led to a 70% decrease in the number of proliferative Ki67(+) NPCs and a 60% reduction in newborn neuron density. Premature loss of GABA(A) depolarization in newborn neurons resulted in truncated dendritic arborization at the time of synaptic integration. However, by 6 weeks the dendritic tree had partially recovered and displayed a small, albeit significant, decrease in dendritic complexity but not total dendritic length. To further examine GABA(A) function on NPCs, we treated animals with a GABA(A) allosteric agonist, pentobarbital. Enhancement of GABA(A) activity in NPCs increased the number of proliferative NPCs by 60%. Combining shNKCC1 and pentobarbital prevented the shNKCC1 and the pentobarbital effects on NPC proliferation, suggesting that these manipulations affected NPCs through GABA(A) receptors. Thus, dysregulation in GABA(A) depolarizing activity delayed dendritic development and reduced NPC proliferation resulting in decreased neuronal density.
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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.