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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.
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).
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