ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Glia-dependent switch of kainate receptor presynaptic action.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Calcium Signaling in Astrocytes and Its Role in the Central Nervous System Injury.Molecular neurobiology · 2025Review
- Two Signaling Modes Are Better than One: Flux-Independent Signaling by Ionotropic Glutamate Receptors Is Coming of Age.Biomedicines · 2024Review
- Control of Long-Term Plasticity by Glutamate Transporters.Frontiers in synaptic neuroscience · 2019Review
- Kainate Receptors Play a Role in Modulating Synaptic Transmission in the Olfactory Bulb.Neuroscience · 2018Article
- Synaptic function and plasticity in identified inhibitory inputs onto VTA dopamine neurons.The European journal of neuroscience · 2018Article
- Phosphatidylinositol 4,5-bisphosphate (PIPThe Journal of physiology · 2017Article
- Article
- Physiological regulation of magnocellular neurosecretory cell activity: integration of intrinsic, local and afferent mechanisms.Journal of neuroendocrinology · 2013Review
- Ionotropic crustacean olfactory receptors.PloS one · 2013Article
- Glial regulation of neuronal function: from synapse to systems physiology.Journal of neuroendocrinology · 2012Review
- Kainate receptor-induced retrograde inhibition of glutamatergic transmission in vasopressin neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Presynaptic kainate receptors (KARs) exert a modulatory action on transmitter release. This effect can be switched from facilitation to inhibition by an increased concentration of KAR agonists. We here report that activation of presynaptic GluK1-containing KARs facilitates GABA release on oxytocin and vasopressin neurons in the supraoptic nucleus of the hypothalamus. Increase in ambient levels of glutamate associated with the physiological reduction of astrocytic coverage of oxytocin neurons in lactating rats switches this KAR-mediated facilitation to inhibition of GABAergic transmission. This effect was reproduced in both oxytocin and vasopressin neurons of virgin rats when glutamate transporters were blocked pharmacologically, thereby establishing that enhanced levels of extracellular glutamate induce the switch in KAR-mediated action. The facilitation of GABA release was inhibited with philanthotoxin, a Ca(2+)-permeable KAR antagonist, suggesting that this effect was associated with an ionotropic mode of action. Conversely, KAR-mediated inhibition was compromised in the presence of U73122, a phospholipase C inhibitor, in agreement with the involvement of a metabotropic pathway. We thus reveal that physiological astrocytic plasticity modifies the mode of action of presynaptic KARs, thereby inversing their coupling with GABA release.
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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.