ArticleThe Journal of physiology2013
SNARE proteins are essential in the potentiation of NMDA receptors by group II metabotropic glutamate receptors.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Pooled it
- Botulinum toxin type A for neuropathic pain in patients with spinal cord injury.Annals of neurology · 2016Trial
- Non-Migraine Head Pain and Botulinum Toxin.Toxins · 2024Review
- Review
- Potential of olfactory neuroepithelial cells as a model to study schizophrenia: A focus on GPCRs (Review).International journal of molecular medicine · 2024Review
- Neuronal SNAP-23 is critical for synaptic plasticity and spatial memory independently of NMDA receptor regulation.iScience · 2023Article
- Review
- SNAP23 regulates KCC2 membrane insertion and activity following mZnR/GPR39 activation in hippocampalneurons.iScience · 2022Article
- The NaCellular and molecular life sciences : CMLS · 2021Article
- Drugs Based on NMDAR Hypofunction Hypothesis in Schizophrenia.Frontiers in neuroscience · 2021Review
- Regulation of NMDA glutamate receptor functions by the GluN2 subunits.Journal of neurochemistry · 2020Review
- The Use of Botulinum Toxin for the Treatment of Chronic Joint Pain: Clinical and Experimental Evidence.Toxins · 2020Review
- Mechanism for neurotransmitter-receptor matching.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- SNARE-Mediated Exocytosis in Neuronal Development.Frontiers in molecular neuroscience · 2020Review
- Postsynaptic RIM1 modulates synaptic function by facilitating membrane delivery of recycling NMDARs in hippocampal neurons.Nature communications · 2018Article
- Targeting metabotropic glutamate receptors for novel treatments of schizophrenia.Molecular brain · 2017Review
- Juvenile treatment with a novel mGluR2 agonist/mGluR3 antagonist compound, LY395756, reverses learning deficits and cognitive flexibility impairments in adults in a neurodevelopmental model of schizophrenia.Neurobiology of learning and memory · 2017Article
- Identification of the SNARE complex mediating the exocytosis of NMDA receptors.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Dysregulations of Synaptic Vesicle Trafficking in Schizophrenia.Current psychiatry reports · 2016Review
- LY395756, an mGluR2 agonist and mGluR3 antagonist, enhances NMDA receptor expression and function in the normal adult rat prefrontal cortex, but fails to improve working memory and reverse MK801-induced working memory impairment.Experimental neurology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The group II metabotropic glutamate receptors (group II mGluRs) have emerged as the new drug targets for the treatment of mental disorders like schizophrenia. To understand the potential mechanisms underlying the antipsychotic effects of group II mGluRs, we examined their impact on NMDA receptors (NMDARs), since NMDAR hypofunction has been implicated in schizophrenia. The activation of group II mGluRs caused a significant enhancement of NMDAR currents in cortical pyramidal neurons, which was associated with increased NMDAR surface expression and synaptic localization. We further examined whether these effects of group II mGluRs are through the regulation of NMDAR exocytosis via SNARE proteins, a family of proteins involved in vesicle fusion. We found that the enhancing effect of APDC, a selective agonist of group II mGluRs, on NMDAR currents was abolished when botulinum toxin was delivered into the recorded neurons to disrupt the SNARE complex. Inhibiting the function of two key SNARE proteins, SNAP-25 and syntaxin 4, also eliminated the effect of APDC on NMDAR currents. Moreover, the application of APDC increased the activity of Rab4, a small Rab GTPase mediating fast recycling from early endosomes to the plasma membrane, and enhanced the interaction between syntaxin 4 and Rab4. Knockdown of Rab4 or expression of dominant-negative Rab4 attenuated the effect of APDC on NMDAR currents. Taken together, these results have identified key molecules involved in the group II mGluR-induced potentiation of NMDAR exocytosis and function.
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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.