ArticleInternational journal of molecular sciences2019
Kainate Receptor-Mediated Depression of Glutamate Release Involves Protein Kinase A in the Cerebellum.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Temporal characterisation and electrophysiological implications of TBI-induced serine/threonine kinase activity in mouse cortex.Cellular and molecular life sciences : CMLS · 2025Article
- Two Signaling Modes Are Better than One: Flux-Independent Signaling by Ionotropic Glutamate Receptors Is Coming of Age.Biomedicines · 2024Review
- Glucagon-like peptide-1 facilitates cerebellar parallel fiber glutamate release through PKA signaling in mice in vitro.Scientific reports · 2023Article
- Focusing on the Emerging Role of Kainate Receptors in the Dorsal Cochlear Nucleus (DCN) and Cerebellum.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
- Cutting-edge genetics in obsessive-compulsive disorder.Faculty reviews · 2020Review
- Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Kainate (KA) receptors (KAR) have important modulatory roles of synaptic transmission. In the cerebellum, the action mechanisms of KAR-mediated glutamatergic depression are unknown. We studied these mechanisms by recording evoked excitatory postsynaptic currents (eEPSCs) from cerebellar slices using the whole-cell configuration of the patch-clamp technique. We observed that 3 μM KA decreased the amplitude of eEPSCs and increased the number of failures at the synapses established between parallel fibers (PF) and Purkinje neurons, and the effect was antagonized by NBQX under the condition where AMPA receptors were previously blocked. The inhibition of protein kinase A (PKA) suppressed the effect of KAR activation on eEPSC, and effect was not prevented by protein kinase C inhibitors. Furthermore, in the presence of Pertussis toxin, the depression of glutamate release mediated by KAR activation was prevented, invoking the participation of a G
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