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The central distribution of AMPARs is absent in GluA3-knockout mice, and gold particles are evenly distributed along the postsynaptic density. GluA4 (show GRIA4 Antibodies) gold labeling was homogenously distributed along both synapse types. Thus, GluA3 and GluA4 (show GRIA4 Antibodies) subunits are distributed at auditory nerve synapses in a target-cell-dependent manner.
The experiments reveal a novel type of plasticity at CA1 (show CA1 Antibodies) hippocampal synapses that is expressed by the activation of GluA3-containing AMPARs.
Results suggest a role for GluA3 channel activity in the regulation of sleep behavior in both mice and humans.
GluA3 is required for normal auditory signaling, normal ultrastructure of AN-BC synapses in the cochlear nucleus and normal experience-dependent changes in auditory processing after transient sound reduction.
These experiments indicate that the presence of GluA3-containing AMPARs is critical for Abeta (show APP Antibodies)-mediated synaptic and cognitive deficits.
Cerebellar learning depends on expression of GluA3 in Purkinje cells. GluA3 is required to induce long term potentiation (LTP (show SCP2 Antibodies)), but not long term depression, at parallel fiber-Purkinje cell synapses. GluA3-dependent potentiation involves a cAMP-driven change in channel conductance. GluA3-mediated LTP (show SCP2 Antibodies) and learning are induced via cAMP-mediated Epac (show RAPGEF3 Antibodies) activation.
These results provide direct evidence for cortical AMPA receptors to contribute to zymosan-induced visceral and spontaneous pain.
Data indicate that the AMPA receptor subunits abundance is hippocampus, GluA2 (show GRIA2 Antibodies) > GluA1 (show GRIA1 Antibodies) > GluA3 >> GluA4 (show GRIA4 Antibodies); cortex, GluA2 (show GRIA2 Antibodies) > GluA3 >/= GluA1 (show GRIA1 Antibodies) >> GluA4 (show GRIA4 Antibodies); and cerebellum, GluA2 (show GRIA2 Antibodies) > GluA3 >/= GluA1 (show GRIA1 Antibodies) > GluA4 (show GRIA4 Antibodies).
This study demonistrated that Gria3 gene expression in mouse dorsal raphe nucleus
This study demonistrated that the GluA3-deficiency in mice is associated with increased social and aggressive behavior and elevated dopamine in striatum.
experiments indicate that mGlu3Delta4 may negatively modulate mGlu3 (show GRM3 Antibodies), and thereby impact on the roles of GRM3/mGlu3 (show GRM3 Antibodies) in schizophrenia and as a therapeutic target
Our findings support the GWAS-implicated link between GRM3 (show GRM3 Antibodies) genetic variation and schizophrenia risk as well as the notion that alleles conferring this risk may be population specific.
Studies support a role for NHERF-1 (show SLC9A3R1 Antibodies) and NHERF-2 (show SLC9A3R2 Antibodies) (Na+/H+ exchanger regulatory factors 1 and 2) in regulating the distribution of Group II metabotropic glutamate (show GRIN1 Antibodies) receptor (mGluRs) in the murine brain, while conversely the effects of the mGluR2 (show GRM2 Antibodies)/3 PDZ (show INADL Antibodies)-binding motifs on receptor signaling are likely mediated by interactions with other PDZ (show INADL Antibodies) scaffold proteins beyond the NHERF (show SLC9A3R1 Antibodies) proteins.
Results demonstrate that GRM3 (show GRM3 Antibodies) expression is significantly upregulated in human colonic adenocarcinomas and colon cancer cell lines. This upregulation is mediated at the post-transcriptional level where miR (show MLXIP Antibodies)-487b directly targets GRM3 (show GRM3 Antibodies) to suppress its translation. Also, the fact that TGFbeta (show TGFB1 Antibodies) increases GRM3 (show GRM3 Antibodies) protein stability provide novel mechanisms of post-transcriptional regulation of GRM3 (show GRM3 Antibodies) in colon cancer.
Low GRM3 (show GRM3 Antibodies) expression is associated with multiple myeloma and B-cell leukemia.
Significant association was found between rs12704290 in GRM3 gene and schizophrenia(SCZ). A three-SNP LD spanning GRM3Delta4 splice site was significantly associated with SCZ. Interaction between the LD block and cognitive function was found in SCZ patients.
Results show that GRM3 (show GRM3 Antibodies) rs274622 C carriers with schizophrenia were associated with significantly smaller prefrontal activation than patients with TT genotype
Grm3 (show GRM3 Antibodies) expression was decreased in B cells from patients with autoimmune diseases such as activated systemic lupus erythematosus and multiple sclerosis.
Pharmacogenetic relationships were identified in patients with schizophrenia between GRM3 (show GRM3 Antibodies) variants and symptom response to antipsychotics.
PI4KA (show PI4KA Antibodies) and GRM3 (show GRM3 Antibodies) polymorphisms have potential to jointly modulate antipsychotic response
L-glutamate is the major excitatory neurotransmitter in the central nervous system and activates both ionotropic and metabotropic glutamate receptors. Glutamatergic neurotransmission is involved in most aspects of normal brain function and can be perturbed in many neuropathologic conditions. The metabotropic glutamate receptors are a family of G protein-coupled receptors, that have been divided into 3 groups on the basis of sequence homology, putative signal transduction mechanisms, and pharmacologic properties. Group I includes GRM1 and GRM5 and these receptors have been shown to activate phospholipase C. Group II includes GRM2 and GRM3 while Group III includes GRM4, GRM6, GRM7 and GRM8. Group II and III receptors are linked to the inhibition of the cyclic AMP cascade but differ in their agonist selectivities.
AMPA-selective glutamate receptor 3
, glutamate receptor 3
, glutamate receptor, ionotrophic, AMPA 3
, glutamate receptor, ionotropic, AMPA3 (alpha 3)
, glutamate receptor channel alpha3 subunit
, glutamate receptor subunit 3
, glutamate metabotropic receptor 3
, metabotropic glutamate receptor 3