ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
N-glycosylation of acid-sensing ion channel 1a regulates its trafficking and acidosis-induced spine remodeling.
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 37 papers.
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Who cites it
37 citing papers in PubMed, 52 citations in OpenAlex.
- Lacking ASIC1a in ASIC4-positive amygdala/bed nucleus of the stria terminalis (BNST) neurons reduces anxiety and innate fear in mice.Journal of biomedical science · 2025Article
- Deciphering distinct spatial alterations in N-glycan expression profiles in the spinal cord and brain of male rats in a neuropathic pain model.Cellular & molecular biology letters · 2025Article
- The gene expression patterns as surrogate indices of pH in the brain.Frontiers in psychiatry · 2023Article
- Thalamocortical circuits drive remifentanil-induced postoperative hyperalgesia.The Journal of clinical investigation · 2022Article
- An induced pluripotent stem cell-derived NMJ platform for study of the NGLY1-Congenital Disorder of Deglycosylation.Advanced therapeutics · 2022Article
- The Mechanisms of Plasticity of Nociceptive Ion Channels in Painful Diabetic Neuropathy.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- ASIC1a is required for neuronal activation via low-intensity ultrasound stimulation in mouse brain.eLife · 2021Article
- Postsynaptic Targeting and Mobility of Membrane Surface-Localized hASIC1a.Neuroscience bulletin · 2021Article
- GPR68 Contributes to Persistent Acidosis-Induced Activation of AGC Kinases and Tyrosine Phosphorylation in Organotypic Hippocampal Slices.Frontiers in neuroscience · 2021Article
- The Role of ASIC1a in Epilepsy: A Potential Therapeutic Target.Current neuropharmacology · 2021Review
- Histidine Residues Are Responsible for Bidirectional Effects of Zinc on Acid-Sensing Ion Channel 1a/3 Heteromeric Channels.Biomolecules · 2020Article
- Factors and Molecular Mechanisms Influencing the Protein Synthesis, Degradation and Membrane Trafficking of ASIC1a.Frontiers in cell and developmental biology · 2020Review
- Selection of an ASIC1a-blocking combinatorial antibody that protects cells from ischemic death.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Human ASIC1a mediates stronger acid-induced responses as compared with mouse ASIC1a.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Endomorphins potentiate acid-sensing ion channel currents and enhance the lactic acid-mediated increase in arterial blood pressure: effects amplified in hindlimb ischaemia.The Journal of physiology · 2017Article
- The glycosylation of the extracellular loop of β2 subunits diversifies functional phenotypes of BK Channels.Channels (Austin, Tex.) · 2017Article
- Region specific contribution of ASIC2 to acidosis-and ischemia-induced neuronal injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- miR-149 reduces while let-7 elevates ASIC1a expression in vitro.International journal of physiology, pathophysiology and pharmacology · 2017Article
- Differential effects of N-linked glycosylation of Vstm5 at multiple sites on surface expression and filopodia formation.PloS one · 2017Article
- Two di-leucine motifs regulate trafficking and function of mouse ASIC2a.Molecular brain · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Acid-sensing ion channel-1a (ASIC1a) is a potential therapeutic target for multiple neurological diseases. We studied here ASIC1a glycosylation and trafficking, two poorly understood processes pivotal in determining the functional outcome of an ion channel. We found that most ASIC1a in the mouse brain was fully glycosylated. Inhibiting glycosylation with tunicamycin reduced ASIC1a surface trafficking, dendritic targeting, and acid-activated current density. N-glycosylation of the two glycosylation sites, Asn393 and Asn366, has differential effects on ASIC1a biogenesis. Maturation of Asn393 increased ASIC1a surface and dendritic trafficking, pH sensitivity, and current density. In contrast, glycosylation of Asn366 was dispensable for ASIC1a function and may be a rate-limiting step in ASIC1a biogenesis. In addition, we revealed that acidosis reduced the density and length of dendritic spines in a time- and ASIC1a-dependent manner. ASIC1a N366Q, which showed increased glycosylation and dendritic targeting, potentiated acidosis-induced spine loss. Conversely, ASIC1a N393Q, which had diminished dendritic targeting and inhibited ASIC1a current dominant-negatively, had the opposite effect. These data tie N-glycosylation of ASIC1a with its trafficking. More importantly, by revealing a site-specific effect of acidosis on dendritic spines, our findings suggest that these processes have an important role in regulating synaptic plasticity and determining long-term consequences in diseases that generate acidosis.
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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.