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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.
GluR2 (show GRIA2 Antibodies) and GluR3 subunits of AMPA receptor play roles in the trigeminal nerve injury-mediated enhancement of neuronal excitability and hyperalgesia.
Mice treated with anti-Glur3 antisense peptide nucleic acids had significantly extended survival compared to mice injected with a nonsense sequence in a mouse model of Amyotrophic lateral sclerosis
By the use of two separate cohorts of mice and by means of two different animal models, namely the cue-induced reinstatement and alcohol deprivation effect paradigms, we could show that the GluR-C subunit is involved in alcohol seeking and relapse.
most important property of GluR2 (show GRIA2 Antibodies) in the context of AMPA receptors trafficking may be its influence on calcium permeability
GluR3 subunits have diverse neurophysiological impact, modulating oscillatory networks for sleep, breathing and seizure generation.
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
Findings suggest that mGluR2 (show GRM2 Antibodies)/3 and mGluR5s are unaltered in the anterior cingulate cortex in psychotic and nonpsychotic depression, bipolar disorder and schizophrenia
Results demonstrate no changes in expression and density of both 5-HT2AR and mGlu2 (show GRM2 Antibodies)/3R in the postmortem prefrontal cortex of subjects with major depressive disorder under basal conditions; antidepressant treatment induces a decrease in 5-HT2AR density
The mGluR3 (show GRM3 Antibodies) promoted the proliferation of human embryonic cortical NPCs and increased cyclin D1 (show CCND1 Antibodies) expression by activating ERK1/2 (show MAPK1/3 Antibodies) and JNK2 (show MAPK9 Antibodies) signaling pathways.
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