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This study showed the lower GluA3 mRNA levels in pregnant women.
the impaired surface expression of homomeric GluA3 receptors is caused by nonproductive assembly and aggregation to which LBD residues Tyr (zeige TYR ELISA Kits)-454 and Arg-461 strongly contribute.
This study demonstrated that the GRIA3 protein was altered in auditory cortex patient with schizophreia.
the levels were comparable for complexes containing GluR2 (zeige GRIA2 ELISA Kits), GluR3 and GluR4 (zeige GRIA4 ELISA Kits) as well as 5-HT1A (zeige HTR1A ELISA Kits). Moreover, the levels of complexes containing muscarinic AChR M1, NR1 (zeige GRIN1 ELISA Kits) and GluR1 (zeige GRIA1 ELISA Kits) were significantly increased in male patients with AD.
An association was observed in migraine patients with the GRIA3 single nucleotide polymorphism rs3761555.
The N-terminal domain modulates alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor desensitization.
The ionotrophic glutamate (zeige GRIN1 ELISA Kits) receptors AMPA3 and AMPA3 were decreased in hippocampus in patient with multiple sclerosis.
The rs557762 and the TT haplotype in the 11th haplotype block of the GRIA3 gene were associated with feelings of guilt in females.
the promoter methylation of the GMR2 and GMR5 genes greatly decreased the risk of schizophrenia, and the expression level of the GRM2 (zeige GRM2 ELISA Kits), GRM5 (zeige GRM5 ELISA Kits), and GRIA3 genes increased significantly in patients in comparison to healthy controls.
GRIA3 plays a role as a mediator of tumor progression in pancreatic cancer downstream CUX1 (zeige CUX1 ELISA Kits).
Cerebellar learning depends on expression of GluA3 in Purkinje cells. GluA3 is required to induce long term potentiation (LTP (zeige SCP2 ELISA Kits)), 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 (zeige SCP2 ELISA Kits) and learning are induced via cAMP-mediated Epac (zeige RAPGEF3 ELISA Kits) 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 (zeige GRIA2 ELISA Kits) > GluA1 (zeige GRIA1 ELISA Kits) > GluA3 >> GluA4 (zeige GRIA4 ELISA Kits); cortex, GluA2 (zeige GRIA2 ELISA Kits) > GluA3 >/= GluA1 (zeige GRIA1 ELISA Kits) >> GluA4 (zeige GRIA4 ELISA Kits); and cerebellum, GluA2 (zeige GRIA2 ELISA Kits) > GluA3 >/= GluA1 (zeige GRIA1 ELISA Kits) > GluA4 (zeige GRIA4 ELISA Kits).
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 (zeige GRIA2 ELISA Kits) 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 (zeige GRIA2 ELISA Kits) 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.
Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. These receptors are heteromeric protein complexes composed of multiple subunits, arranged to form ligand-gated ion channels. The classification of glutamate receptors is based on their activation by different pharmacologic agonists. The subunit encoded by this gene belongs to a family of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate)-sensitive glutamate receptors, and is subject to RNA editing (AGA->GGA\; R->G). Alternative splicing at this locus results in different isoforms, which may vary in their signal transduction properties.
glutamate receptor, ionotrophic, AMPA 3
, glutamate receptor, ionotropic, AMPA 3.2
, glutamate receptor C
, AMPA receptor GluR3/C
, glutamate receptor subunit AMPA3
, glutamate receptor 3
, AMPA GluR3
, Glutamate receptor 3-like
, glutamate receptor 3-like
, AMPA-selective glutamate receptor 3
, glutamate receptor, ionotropic, AMPA3 (alpha 3)
, glutamate receptor subunit 3
, glutamate receptor channel alpha3 subunit