he current study investigated novel curcumin derivatives on the biophysical properties of AMPA receptors specifically on the homomeric GluA2 and the heteromeric GluA2/A3 subunits and assessed for inhibitory actions
Study reports heterozygous de novo GRIA2 mutations in 28 unrelated patients with intellectual disability and neurodevelopmental abnormalities. When GluA2 subunits are co-expressed with GluA1 most GRIA2 mutations cause a decreased current amplitude and some also affect voltage rectification.
Nanoscale mobility of resting AMPA receptors predetermines responsiveness to neurotransmitter allosteric anions and TARP auxiliary subunits. Mobility at rest is regulated by alternative splicing of the flip/flop cassette of the ligand-binding domain which controls motions in the distant AMPA receptor N-terminal domain (NTD).
a dramatic reduction of expression of the GluA2 subunit occurs concomitantly with its hyper-phosphorylation on Serine 880 and increased ubiquitination. Consequently Cdkl5 silencing skews the composition of membrane-inserted AMPA-Rs towards the GluA2-lacking calcium-permeable form
Reduced expression of Gria2 increased Ca(2+) influx through Ca(2+)-permeable AMPA receptors which increased the vulnerability and affected the differentiation and migration of distinct cell populations and interfered with normal circuit formation in fragile X syndrome.
Measured the expression of GRIA2 and GABRA1 in patients with methamphetamine-use disorder. Also examined whether miR-181a down-regulates GRIA2 and GABRA1 in a cell-based assay. We further examined the effects of chronic methamphetamine exposure on the expression of miR-181a GRIA2 and GABRA1. The results demonstrated that serum GRIA2 is higher in patients with methamphetamine-use disorder than in healthy controls.
both the intracellular C-terminal domain (CTD) and the loop region between the M1 and M2 helices move during activation and the CTD is detached from the membrane
A transient positive feedback mechanism between AMPAR and stargazin has implications for information processing in the brain because it should allow activity-dependent facilitation of excitatory synaptic transmission through a postsynaptic mechanism.
GRIA2*CCC polymorphism is genetic risk marker for paranoid schizophrenia in Russians.Low risk genetic markers of paranoid schizophrenia were revealed: in Tatars-GRIA2*T/T (rs43025506) of GRIA2 gene and GRIA2*CCT in Russians.
We show that excitatory cortical-patterned neurons derived from multiple human pluripotent stem cell lines exhibit native-like maturation changes in AMPAR composition such that there is an increase in the expression of GluA2(R) subunits.
analysis of changes in receptor kinetics with the R628E charge-inverting mutation in the "linker" region of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor
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.
The data potentially suggest a lack of epistatic interaction between GRIA2 and GRIA4 variants regarding clinical outcomes in patients with major depressive disorder.
Studies indicate that AMPAR trafficking is a key mechanism that drives nascent synapse development and is the main determinant of both Hebbian and homeostatic plasticity in mature synapses.
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