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Stau2 downregulation (Stau2(GT)) led to an increase of glutamate receptor ionotropic delta subunit 2 (GluD2) in Purkinje cells when animals performed physical activity by voluntary wheel running compared with the age-matched wildtype (WT) mice (C57Bl/6J).
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GLUD2 transgenic mice were generated by inserting in their genome, a segment of the human X chromosome containing the GLUD2 gene and its promoter.
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Results suggest that the GluRdelta2 receptor plays an important role in the long-term organization of the granule-Purkinje cell circuit through its involvement in the regulation of parallel fiber-Purkinje cell synaptogenesis and in the normal functioning of this critical cerebellar circuit.
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The GluD2 mutation in the ho15J mice affects stable retention of the acquired conditioned bradycardia.
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Notably, the introduction of GLUD2 did not affect glutamate levels in mice, consistent with observations in the primates. Instead, the metabolic effects of GLUD2 center on the tricarboxylic acid cycle, suggesting that GLUD2 affects carbon flux during early brain development, possibly supporting lipid biosynthesis.
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This study showed that spontaneous Grid2 mutations causing cerebellar pathology are impaired in motor functions during the neonatal period.
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Established is a mouse line with an autosomal recessive gene mutation characterized by progressive ataxia and significant cerebellar atrophy.
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GluD2 works in concert with GluD1 for the construction of cerebellar synaptic wiring through distinct neuronal and synaptic expressions.
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Climbing fiber signals in Glu2 receptor delta2 knock-out mice propagate across multiple microzones.
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GluD2 deletion impairs presynaptic R-type voltage-gated Ca(2+) channels, resulting in decreased release of synaptic vesicles
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The results suggest that multiple PC death pathways are induced by the physical trauma of making organotypic slice cultures, naturally-occurring postnatal cell death, and the GluRdelta2 (Lc) mutation.
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CD95 and soluble CD95L contribute, via non-apoptotic signaling, to the inflammatory reaction initiated early in neuron death within the Grid2(Lc/+) cerebellum
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activity-dependent phosphorylation of serine 880 (S880) in GluA2 AMPA receptor subunit, which is an essential step for AMPA receptor endocytosis during LTD induction, was impaired in GluD2-null cerebellum
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GluRdelta2 is part of the mGluR1 signaling complex needed for cerebellar synaptic function and motor coordination
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[review] The Cbln1-GluRdelta2 receptor complex is located at the cleft of parallel fiber-Purkinje cell synapses and bidirectionally regulates both presynaptic and postsynaptic differentiation.
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[review] GluRdelta2 plays critical roles in formation, maturation, and/or maintenance of granule neuron-Purkinje neuron synapses.
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These results indicate that glial D-Ser regulates synaptic plasticity and cerebellar functions by interacting with GluD2.
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It is a molecule involved in synaptic plasticity in the cerebellum. (review)
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GluRdelta2 fuels heterosynaptic competition and gives purkinje fibers the competitive advantages over climbing fibers throughout the animal's life.
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Results suggest that GluRdelta2 mediates cerebellar synapse formation by interacting with presynaptic NRXNs through Cbln1.