Expression of GluR6 kainate receptor subunit in granular layer of weaver mouse cerebellum

Spiliopoulos, Konstantinos; Fragioudaki, K.; Giompres, Panagiotis; Kouvelas, Elias D.; Mitsacos, Ada

doi:10.1007/s00702-009-0199-8

Cited by 3 publications

(5 citation statements)

References 24 publications

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“…iGluRs are divided into NMDA (N‐methyl‐D‐aspartic acid receptor) receptors, AMPA receptors and KAR (kainate receptor) according to their preferred ligands. KAR is a tetrameric receptor molecule composed of five subunits, including GluR5, GluR6, GluR7, KAR1, and KAR2 135 . The sodium alginate receptor GluR6 subunit is widely expressed throughout the brain and is most abundant in the hippocampus.…”

Section: Channelopathymentioning

confidence: 99%

“…KAR is a tetrameric receptor molecule composed of five subunits, including GluR5, GluR6, GluR7, KAR1, and KAR2. 135 The sodium alginate receptor GluR6 subunit is widely expressed throughout the brain and is most abundant in the hippocampus. GluR6 plays important roles in synaptic plasticity, learning and memory, and epilepsy by regulating the excitability of presynaptic and postsynaptic neurons.…”

Section: Glutamate Receptor 6 (Glur6)mentioning

confidence: 99%

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The function of SUMOylation and its crucial roles in the development of neurological diseases

et al. 2021

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Neurological diseases are relatively complex diseases of a large system; however, the detailed mechanism of their pathogenesis has not been completely elucidated, and effective treatment methods are still lacking for some of the diseases. The SUMO (small ubiquitin‐like modifier) modification is a dynamic and reversible process that is catalyzed by SUMO‐specific E1, E2, and E3 ligases and reversed by a family of SENPs (SUMO/Sentrin‐specific proteases). SUMOylation covalently conjugates numerous cellular proteins, and affects their cellular localization and biological activity in numerous cellular processes. A wide range of neuronal proteins have been identified as SUMO substrates, and the disruption of SUMOylation results in defects in synaptic plasticity, neuronal excitability, and neuronal stress responses. SUMOylation disorders cause many neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease. By modulating the ion channel subunit, SUMOylation imbalance is responsible for the development of various channelopathies. The regulation of protein SUMOylation in neurons may provide a new strategy for the development of targeted therapeutic drugs for neurodegenerative diseases and channelopathies.

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Section: Channelopathymentioning

confidence: 99%

Section: Glutamate Receptor 6 (Glur6)mentioning

confidence: 99%

The function of SUMOylation and its crucial roles in the development of neurological diseases

et al. 2021

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“…As indicated above, KARs are expressed in the cerebellar cortex [57][58][59]. As known, the cerebellum participates in the modulation of movement by modifying the activity patterns of motor neurons.…”

Section: Kars In the Cerebellummentioning

confidence: 99%

Kainate Receptors Modulating Glutamate Release in the Cerebellum

Losada-Ruiz¹,

Falcón-Moya²,

Rodríguez‐Moreno³

2019

Biogenic Amines in Neurotransmission and Human Disease

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Glutamate receptors of the kainate type (Kainate receptors, KARs), are mediators of ionotropic postsynaptic synaptic transmission, as well as presynaptic modulators of neurotransmitter release where they show both ionotropic and metabotropic actions regulating glutamate and γ-aminobutiric acid (GABA) release. The mechanisms underlying these modulatory roles are starting to be understood at some brain regions. Here we review the KARs roles and mechanisms involved in the modulation of glutamate release in the cerebellum at parallel fibers (PF)-Purkinje Cells (PuC) synapses. KARs activation mediate a biphasic effect on glutamate release at this synapse, with low kainate (KA) concentrations mediating a facilitation of glutamate release and higher KA concentrations mediating a depression of glutamate release. KA-mediated facilitation is prevented by antagonizing KARs, by inhibition of PKA or stimulation of adenylyl cyclase (AC), by blocking Ca 2+ permeant KARs, by depleting intracellular Ca 2+ stores and by blocking calmodulin. Thus, at cerebellar parallel fiber-Purkinje cell synapses, presynaptic KARs mediate glutamate release facilitation through Ca 2+-calmodulin dependent activation of adenylyl cyclase/cAMP/protein kinase A signaling. KAR-mediated depression of glutamate release involves the AC/cAMP/PKA pathway as for facilitation but not Ca 2+-calmodulin, being in this case AC activated by a Gi/o protein to mediate a depression of glutamate release.

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“…After considerable effort, we finally devised a synthesis of [vinylidene‐ 3 H]kainic acid using a protected ketone precursor and a tritiated Wittig reagent . Several hundred published studies have used [ 3 H]kainic acid to date …”

Section: Marine Toxin Alkaloidsmentioning

confidence: 99%

“…178 Several hundred published studies have used [ 3 H]kainic acid to date. 179,180 14 | CONCLUSION Perhaps no other class of natural products has such a diverse array of sources, structures, and applications as the thousands of known alkaloids. Clearly, the extreme structural and functional variety of alkaloids has presented both valuable opportunities and complex synthetic challenges for their tritiation.…”

Section: Marine Toxin Alkaloidsmentioning

confidence: 99%