Non-canonical mechanisms of presynaptic kainate receptors controlling glutamate release
Open accessAbstract
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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At mossy fiber synapses connecting DG and CA3, kainate receptors inhibit glutamatergic signaling when glutamate is released at high levels, while facilitating release at lower levels, via a Gi/o-coupled mechanism.
“At mossy fiber synapses connecting DG and CA3 (areas of high kainate receptor expression throughout life), kainate receptors inhibit glutamatergic signaling when glutamate is released at high levels, while facilitating release at lower levels, again via a G i/o -coupled mechanism (Negrete-Díaz et al., 2018).”
From Glutamate receptors in domestication and modern human evolution (2020) · cites this paper as Negrete-Díaz et al., 2018
Kainate receptor activation at CA3-CA1 synapses serves to inhibit glutamate transmission via Gi/o signaling, especially when synapses are immature.
“Kainate receptor activation at CA3-CA1 synapses serves to inhibit glutamate transmission via G i/o signaling, especially when synapses are immature.”
From Glutamate receptors in domestication and modern human evolution (2020) · cites this paper as Negrete-Díaz et al., 2018
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Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels
Hansen, K. B., Wollmuth, L. P., Bowie, D., Furukawa, H., Menniti, F. S., Sobolevsky, A. I., Swanson, G. T., Swanger, S. A., Greger, I. H., Nakagawa, T., et al. (2021) · Pharmacological Reviews · doi:10.1124/pharmrev.120.000131 · Cited by 686 · see citing works
Glutamate receptors in domestication and modern human evolution
O’Rourke, T., & Boeckx, C. (2020) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2019.10.004 · Cited by 50 · see citing works
- Authors
- Negrete-Díaz, J. V., Sihra, T. S., Flores, G., & Rodríguez-Moreno, A.
- Affiliations
- University College London (GB)
- Benemérita Universidad Autónoma de Puebla (MX)
- ORCID
- Flores, Gonzalo
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-04-20
- Volume
- 11
- Pages
- 128-128
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC5920280
- OpenAlex
- W2799475388
- Cited by
- 41
- References
- 82
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 6 · 2021: 12 · 2020: 4 · 2019: 9 · 2018: 4
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Ministerio de Economàa y Competitividad (BFU2006-14155, BFU2009-10034, BFU2012-38208)
- Consejeràa de Economàa, Innovación, Ciencia y Empleo, Junta de Andalucàa (CVI-7290)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Keywords
- kainate receptors, presynaptic modulation, glutamate release, metabotropic signaling, G protein signaling, protein kinase A, adenylate cyclase, glutamatergic neurotransmission
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