Paternal stress alters synaptic density and expression of GAP-43 GRIN1 M1 and SYP genes in the hippocampus and cortex of offspring of stress-induced male rats.
Involuntary forced or voluntary exercise can ameliorate the cognitive deficits by enhancing levels of hippocampal NMDAR1 pAMPAR1 and pCaMKII in a model of vascular dementia.
In aged rats overall decreases in NR1 NR2A and NR2B expression and reduction in neuronal and endothelial NOS activities in the rat cerebral cortex were found. The age-dependent changes in NR1 and NR2B correlated with neuronal NOS in both hemispheres. The effect of sleep deprivation was also studied.
Social isolation rearing of rats throughout adolescence results in decreased density of GluN1 in dopamine-receptive dendrites of the nucleus accumbens core.
Chronic unpredictable mild stress rats had significantly higher expression levels of the NMDAR subunits GluN1 in the paraventricular nucleus than unstressed rats.
Allosteric interactions occur between the glutamate-binding GluN2 subunits in triheteromeric GluN1/2A/2B NMDARs. This allosterism is dominated by the GluN2A subunit and results in functional properties not predicted by those of diheteromeric GluN1/2A and GluN1/2B NMDARs.
The relative gene expression of rostral ventral lateral medulla (RVLM) NMDA and AMPA glutamate-gated receptor subunits and protein concentration of select receptor subunits did not differ between young and aged rats and there were no age-related differences in the expression of RVLM ionotropic GABAA and Gly receptors or of protein concentration of select GABAA subunits.
tPA is a ligand of the N-terminal domain of the obligatory GluN1 subunit of NMDAR acting as a modulator of their dynamic distribution at the neuronal surface and subsequent signaling.
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