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Frontotemporal dementia patients manifest significant reduction of the GluR3 subunit in the postsynaptic fraction due to autoantibodies along with increased levels of neuronal Tau.
Results suggest a role for GluA3 channel activity in the regulation of sleep behavior in both mice and humans.
miR-330-3p up-regulated the total DNA methylation in non-small cell lung cancer cells, and co-IP-demonstrated GRIA3 was directly related with DNMT1 and DNMT3A. GRIA3 is a direct target of miR-330-3p.
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-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, GluR3 and GluR4 as well as 5-HT1A. Moreover, the levels of complexes containing muscarinic AChR M1, NR1 and GluR1 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 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, GRM5, and GRIA3 genes increased significantly in patients in comparison to healthy controls.
SNP rs687577 associated with sleep duration and depression risk in Finnish women
GRIA3 plays a role as a mediator of tumor progression in pancreatic cancer downstream CUX1.
Two variants in the regulative regions of GRIA1 (rs2195450) and GRIA3 (rs3761555) genes resulted strongly associated with MA (P = 0.00002 and P = 0.0001, respectively), but not associated with MO
AQP3 gene isn't the responsible gene for this pedigree with auditory neuropathy.
This study demonistrated that the level of metabotropic glutamate receptor 2/3 is elevated in the prefrontal cortex in patient of major depression disorder.
The mGlu3 receptor is located on a number of GABAergic interneurons throughout the brain. mGlu3 receptor is one of two primary mGlu receptors that modulate the function of glia. The mGlu3 receptor is present as a postsynaptic receptor as well.
Flip and flop splice variants of AMPA receptor subunits in the spinal cord of amyotrophic lateral sclerosis.
T lymphocytes from normal individuals, an alloprimed human T cell clone, and human T leukemia (Jurkat) cells all express high levels of GluR3, identical in sequence with brain GluR3.
The central distribution of AMPARs is absent in GluA3-knockout mice, and gold particles are evenly distributed along the postsynaptic density. GluA4 gold labeling was homogenously distributed along both synapse types. Thus, GluA3 and GluA4 subunits are distributed at auditory nerve synapses in a target-cell-dependent manner.
The experiments reveal a novel type of plasticity at CA1 hippocampal synapses that is expressed by the activation of GluA3-containing AMPARs.
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-mediated synaptic and cognitive deficits.
Cerebellar learning depends on expression of GluA3 in Purkinje cells. GluA3 is required to induce long term potentiation (LTP), 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 and learning are induced via cAMP-mediated Epac 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 > GluA1 > GluA3 >> GluA4; cortex, GluA2 > GluA3 >/= GluA1 >> GluA4; and cerebellum, GluA2 > GluA3 >/= GluA1 > GluA4.
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 and GluR3 subunits of AMPA receptor play roles in the trigeminal nerve injury-mediated enhancement of neuronal excitability and hyperalgesia.
limited proteolysis is another post-translational mechanism through which functional diversity and specialization between closely related GluR subunits is accomplished
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 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.
MCT2 is linked to AMPA receptor GluR2/3 subunits and undergoes a similar translocation process in neurons upon activation
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