ArticleHistochemistry and cell biology2016
KCC2 knockdown impairs glycinergic synapse maturation in cultured spinal cord neurons.
Article in Histochemistry and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Characterization of optogenetically activated inhibitory inputs onto cholinergic motor neurons in the spinal dorsolateral nucleus.Physiological reports · 2025Article
- Unraveling the socio-cognitive consequences of KCC2 disruption in zebrafish: implications for neurodevelopmental disorders and therapeutic interventions.Frontiers in molecular neuroscience · 2024Article
- Startle Disease: New Molecular Insights into an Old Neurological Disorder.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2023Review
- Glycine neurotransmission: Its role in development.Frontiers in neuroscience · 2022Review
- Anxiety and Startle Phenotypes inFrontiers in molecular neuroscience · 2020Article
- A Brain Signaling Framework for Stress-Induced Depression and Ketamine Treatment Elucidated by Phosphoproteomics.Frontiers in cellular neuroscience · 2020Article
- Assembly and maintenance of GABAergic and Glycinergic circuits in the mammalian nervous system.Neural development · 2018Review
- Investigating the Mechanism by Which Gain-of-function Mutations to the α1 Glycine Receptor Cause Hyperekplexia.The Journal of biological chemistry · 2016Article
- Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic inhibition in the spinal cord is mediated mainly by strychnine-sensitive glycine (GlyRs) and by γ-aminobutyric acid type A receptors (GABAAR). During neuronal maturation, neonatal GlyRs containing α2 subunits are replaced by adult-type GlyRs harboring α1 and α3 subunits. At the same time period of postnatal development, the transmembrane chloride gradient is changed due to increased expression of the potassium-chloride cotransporter (KCC2), thereby shifting the GABA- and glycine-mediated synaptic currents from mostly excitatory depolarization to inhibitory hyperpolarization. Here, we used RNA interference to suppress KCC2 expression during in vitro maturation of spinal cord neurons. Morphological analysis revealed reduced numbers and size of dendritic GlyR clusters containing α1 subunits but not of clusters harboring neonatal α2 subunits. The morphological changes were accompanied by decreased frequencies and amplitudes of glycinergic miniature inhibitory currents, whereas GABAergic synapses appeared functionally unaltered. Our data indicate that KCC2 exerts specific functions for the maturation of glycinergic synapses in cultured spinal cord neurons.
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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.