ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
In the developing rat hippocampus, endogenous activation of presynaptic kainate receptors reduces GABA release from mossy fiber terminals.
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 14 papers.
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14 citing papers in PubMed, 28 citations in OpenAlex.
- GluK1 kainate receptors in parvalbumin interneurons modulate cortico-hippocampal network dynamics during social behavior.Translational psychiatry · 2026Article
- The Role of Calcium-Permeable Kainate and AMPA Receptors in the Leading Reaction of GABAergic Neurons to Excitation.Current issues in molecular biology · 2026Article
- Properties of GABAergic Neurons Containing Calcium-Permeable Kainate and AMPA-Receptors.Life (Basel, Switzerland) · 2021Article
- The Role of Phospholipase C in GABAergic Inhibition and Its Relevance to Epilepsy.International journal of molecular sciences · 2021Review
- Electrophysiological characterization of granule cells in the dentate gyrus immediately after birth.Frontiers in cellular neuroscience · 2014Article
- Mixed neurotransmission in the hippocampal mossy fibers.Frontiers in cellular neuroscience · 2013Review
- PrPC controls via protein kinase A the direction of synaptic plasticity in the immature hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Fluoxetine impairs GABAergic signaling in hippocampal slices from neonatal rats.Frontiers in cellular neuroscience · 2013Article
- Deficits in morphofunctional maturation of hippocampal mossy fiber synapses in a mouse model of intellectual disability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Expression of GluK1c underlies the developmental switch in presynaptic kainate receptor function.Scientific reports · 2012Article
- Developmental regulation of CB1-mediated spike-time dependent depression at immature mossy fiber-CA3 synapses.Scientific reports · 2012Article
- Enhanced Synaptic Activity and Epileptiform Events in the Embryonic KCC2 Deficient Hippocampus.Frontiers in cellular neuroscience · 2011Article
- Phenobarbital but Not Diazepam Reduces AMPA/kainate Receptor Mediated Currents and Exerts Opposite Actions on Initial Seizures in the Neonatal Rat Hippocampus.Frontiers in cellular neuroscience · 2011Article
- Control of GABA Release at Mossy Fiber-CA3 Connections in the Developing Hippocampus.Frontiers in synaptic neuroscience · 2010Article
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3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Presynaptic kainate receptors regulate synaptic transmission in several brain areas but are not known to have this action at immature mossy fiber (MF) terminals, which during the first week of postnatal life release GABA, which exerts into targeted cells a depolarizing and excitatory action. Here, we report that, during the first week of postnatal life, endogenous activation of GluK1 receptors by glutamate present in the extracellular space severely depresses MF-mediated GABAergic currents [GABA(A)-mediated postsynaptic currents (GPSCs)]. Activation of GluK1 receptors was prevented by treating the slices with enzymatic glutamate scavengers that enhanced the clearance of glutamate from the extracellular space. The depressant effect of GluK1 on MF-GPSCs was mediated by a metabotropic process sensitive to pertussis toxin. In the presence of U73122 (1-[6-[[(17b)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione), a selective inhibitor of phospholipase C, along the transduction pathway downstream to G-protein, GluK1 activation increased the probability of GABA release, thus unveiling the ionotropic action of this receptor. In line with this type of action, we found that GluK1 enhanced MF excitability by directly depolarizing MF terminals via calcium-permeable cation channels. Furthermore, GluK1 dynamically regulated the direction of spike time-dependent plasticity occurring by pairing MF stimulation with postsynaptic spiking and switched spike time-dependent potentiation into depression. The GluK1-induced depression of MF-GPSCs would prevent excessive activation of the CA3 associative network by the excitatory action of GABA and the emergence of seizures in the immature brain.
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