ReviewFrontiers in molecular neuroscience2018
Non-canonical Mechanisms of Presynaptic Kainate Receptors Controlling Glutamate Release.
Review in Frontiers in molecular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- Isolation, characterization and testing of RNA aptamers targeting glutamate receptors in a rat spinal cord injury pain model.Communications biology · 2025Article
- Kainate receptors in the CA2 region of the hippocampus.Neural regeneration research · 2023Article
- Kainate Receptor Antagonists: Recent Advances and Therapeutic Perspective.International journal of molecular sciences · 2023Review
- Efavirenz restored NMDA receptor dysfunction and inhibited epileptic seizures inFrontiers in neuroscience · 2023Article
- Kainate receptor subunit 1 (GRIK1) risk variants and GRIK1 deficiency were detected in the Indian ADHD probands.Scientific reports · 2022Article
- Discovery of the First Highly Selective Antagonist of the GluK3 Kainate Receptor Subtype.International journal of molecular sciences · 2022Article
- ATM rules neurodevelopment and glutamatergic transmission in the hippocampus but not in the cortex.Cell death & disease · 2022Article
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- Ionotropic Receptors as a Driving Force behind Human Synapse Establishment.Molecular biology and evolution · 2021Article
- Neuron-specific spinal cord translatomes reveal a neuropeptide code for mouse dorsal horn excitatory neurons.Scientific reports · 2021Article
- Zinc Modulates Olfactory Bulb Kainate Receptors.Neuroscience · 2020Article
- Damaging coding variants within kainate receptor channel genes are enriched in individuals with schizophrenia, autism and intellectual disabilities.Scientific reports · 2019Article
- The glutamate receptor GluK2 contributes to the regulation of glucose homeostasis and its deterioration during aging.Molecular metabolism · 2019Article
- Kainate Receptor-Mediated Depression of Glutamate Release Involves Protein Kinase A in the Cerebellum.International journal of molecular sciences · 2019Article
- Development of Cortical Pyramidal Cell and Interneuronal Dendrites: a Role for Kainate Receptor Subunits and NETO1.Molecular neurobiology · 2019Article
- NMDA Receptors Containing GluN2B/2C/2D Subunits Mediate an Increase in Glutamate Release at Hippocampal CA3-CA1 Synapses.Molecular neurobiology · 2019Article
- Kainate Receptors Play a Role in Modulating Synaptic Transmission in the Olfactory Bulb.Neuroscience · 2018Article
- Review
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Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A metabotropic modus operandi for kainate receptors (KARs) was first discovered in 1998 modulating GABA release. These receptors have been also found to modulate glutamate release at different synapses in several brain regions. Mechanistically, a general biphasic mechanism for modulating glutamate release by presynaptic KARs with metabotropic actions has emerged, with low KA concentrations invoking an increase in glutamate release, whereas higher concentrations of KA mediate a decrease in the release of this neurotransmitter. The molecular mechanisms underpinning the opposite modulation of glutamate release are distinct, with a G-protein-independent, adenylate cyclase (AC)- and protein kinase A (PKA)-dependent mechanism mediating the facilitation of glutamate release, while a G-protein dependent mechanism (with or without protein kinase recruitment) is involved in the decrease of neurotransmitter release. In the present review, we revisit the mechanisms underlying the non-canonical modus operandi of KARs effecting the bimodal control of glutamatergic transmission in different brain regions, and address the possible functions that this modulation may support.
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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.