ArticleFrontiers in cellular neuroscience2016
Axonal Kainate Receptors Modulate the Strength of Efferent Connectivity by Regulating Presynaptic Differentiation.
Article in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- The Role of Calcium-Permeable Kainate and AMPA Receptors in the Leading Reaction of GABAergic Neurons to Excitation.Current issues in molecular biology · 2026Article
- Aberrant glycosylation in schizophrenia: insights into pathophysiological mechanisms and therapeutic potentials.Frontiers in pharmacology · 2024Review
- Review
- Focusing on the Emerging Role of Kainate Receptors in the Dorsal Cochlear Nucleus (DCN) and Cerebellum.International journal of molecular sciences · 2023Review
- ATM rules neurodevelopment and glutamatergic transmission in the hippocampus but not in the cortex.Cell death & disease · 2022Article
- Properties of GABAergic Neurons Containing Calcium-Permeable Kainate and AMPA-Receptors.Life (Basel, Switzerland) · 2021Article
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- Kainate receptors regulate the functional properties of young adult-born dentate granule cells.Cell reports · 2021Article
- Kainate receptors regulate development of glutamatergic synaptic circuitry in the rodent amygdala.eLife · 2020Article
- The Kainate Receptor Subunit GluK2 Interacts With KCC2 to Promote Maturation of Dendritic Spines.Frontiers in cellular neuroscience · 2020Article
- NETO1 Regulates Postsynaptic Kainate Receptors in CA3 Interneurons During Circuit Maturation.Molecular neurobiology · 2019Article
- Exciting Times: New Advances Towards Understanding the Regulation and Roles of Kainate Receptors.Neurochemical research · 2019Review
- Non-canonical Mechanisms of Presynaptic Kainate Receptors Controlling Glutamate Release.Frontiers in molecular neuroscience · 2018Review
- Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kainate type of glutamate receptors (KARs) are highly expressed during early brain development and may influence refinement of the circuitry, via modulating synaptic transmission and plasticity. KARs are also localized to axons, however, their exact roles in regulating presynaptic processes remain controversial. Here, we have used a microfluidic chamber system allowing specific manipulation of KARs in presynaptic neurons to study their functions in synaptic development and function in vitro. Silencing expression of endogenous KARs resulted in lower density of synaptophysin immunopositive puncta in microfluidically isolated axons. Various recombinant KAR subunits and pharmacological compounds were used to dissect the mechanisms behind this effect. The calcium permeable (Q) variants of the low-affinity (GluK1-3) subunits robustly increased synaptophysin puncta in axons in a manner that was dependent on receptor activity and PKA and PKC dependent signaling. Further, an associated increase in the mean active zone length was observed in electron micrographs. Selective presynaptic expression of these subunits resulted in higher success rate of evoked EPSCs consistent with higher probability of glutamate release. In contrast, the calcium-impermeable (R) variant of GluK1 or the high-affinity subunits (GluK4,5) had no effect on synaptic density or transmission efficacy. These data suggest that calcium permeable axonal KARs promote efferent connectivity by increasing the density of functional presynaptic release sites.
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