ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Na+/K+-ATPase is a new interacting partner for the neuronal glycine transporter GlyT2 that downregulates its expression in vitro and in vivo.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Role of the Glycine Transporter GlyT2 in the Neuronal Differentiation of PC12 Cells.International journal of molecular sciences · 2026Article
- A New GlyT2 Variant Associated with Hyperekplexia.International journal of molecular sciences · 2025Article
- Impaired Presynaptic Function Contributes Significantly to the Pathology of Glycine Receptor Autoantibodies.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Monitoring of activity-driven trafficking of endogenous synaptic proteins through proximity labeling.PLoS biology · 2024Article
- Calcium-Dependent Regulation of the Neuronal Glycine Transporter GlyT2 by M2 Muscarinic Acetylcholine Receptors.Neurochemical research · 2022Article
- The presynaptic glycine transporter GlyT2 is regulated by the Hedgehog pathway in vitro and in vivo.Communications biology · 2021Article
- Article
- Ouabain-Induced Gene Expression Changes in Human iPSC-Derived Neuron Culture Expressing Dopamine and cAMP-Regulated Phosphoprotein 32 and GABA Receptors.Brain sciences · 2021Article
- A System for Assessing Dual Action Modulators of Glycine Transporters and Glycine Receptors.Biomolecules · 2020Article
- E3 ubiquitin ligases LNX1 and LNX2 are major regulators of the presynaptic glycine transporter GlyT2.Scientific reports · 2019Article
- Article
- Multiple myosin motors interact with sodium/potassium-ATPase alpha 1 subunits.Molecular brain · 2018Article
- Neuronal Porosome Complex: Secretory Machinery at the Nerve Terminal.Discoveries (Craiova, Romania) · 2017Review
- Glycinergic transmission: glycine transporter GlyT2 in neuronal pathologies.Neuronal signaling · 2017Review
- A novel de novo mutation in ATP1A3 and childhood-onset schizophrenia.Cold Spring Harbor molecular case studies · 2016Article
- The neuronal porosome complex in health and disease.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- Insights into the Pathology of the α3 Na(+)/K(+)-ATPase Ion Pump in Neurological Disorders; Lessons from Animal Models.Frontiers in physiology · 2016Review
- Specialized Functional Diversity and Interactions of the Na,K-ATPase.Frontiers in physiology · 2016Review
- Insights into the Pathology of the α2-Na(+)/K(+)-ATPase in Neurological Disorders; Lessons from Animal Models.Frontiers in physiology · 2016Review
- α-synuclein assemblies sequester neuronal α3-Na+/K+-ATPase and impair Na+ gradient.The EMBO journal · 2015Article
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neuronal glycine transporter GlyT2 plays a fundamental role in the glycinergic neurotransmission by recycling the neurotransmitter to the presynaptic terminal. GlyT2 is the main supplier of glycine for vesicle refilling, a process that is absolutely necessary to preserve quantal glycine content in synaptic vesicles. Alterations in GlyT2 activity modify glycinergic neurotransmission and may underlie several neuromuscular disorders, such as hyperekplexia, myoclonus, dystonia, and epilepsy. Indeed, mutations in the gene encoding GlyT2 are the main presynaptic cause of hyperekplexia in humans and produce congenital muscular dystonia type 2 (CMD2) in Belgian Blue cattle. GlyT2 function is strictly coupled to the sodium electrochemical gradient actively generated by the Na+/K+-ATPase (NKA). GlyT2 cotransports 3Na+/Cl-/glycine generating large rises of Na+ inside the presynaptic terminal that must be efficiently reduced by the NKA to preserve Na+ homeostasis. In this work, we have used high-throughput mass spectrometry to identify proteins interacting with GlyT2 in the CNS. NKA was detected as a putative candidate and through reciprocal coimmunoprecipitations and immunocytochemistry analyses the association between GlyT2 and NKA was confirmed. NKA mainly interacts with the raft-associated active pool of GlyT2, and low and high levels of the specific NKA ligand ouabain modulate the endocytosis and total expression of GlyT2 in neurons. The ouabain-mediated downregulation of GlyT2 also occurs in vivo in two different systems: zebrafish embryos and adult rats, indicating that this NKA-mediated regulatory mechanism is evolutionarily conserved and may play a relevant role in the physiological control of inhibitory glycinergic neurotransmission.
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