GLUR2/3 antibodies have elucidated critical roles of AMPA receptors in neurobiology and pathology:
Alzheimer’s Disease: Loss of GLUR2/3 immunoreactivity precedes neurofibrillary tangle formation in entorhinal cortex neurons. Double-labeling studies show no co-localization with early cytoskeletal markers (e.g., MC1), suggesting GLUR2/3 dysfunction is an early pathological event .
Cocaine-Induced Plasticity: Chronic cocaine exposure alters GLUR2/3 expression in the nucleus accumbens, contributing to addiction-related synaptic remodeling .
AMPA Receptor Desensitization: The N-terminal domain of GLUR2/3 modulates receptor desensitization kinetics, influencing synaptic strength .
Encephalitis Mechanisms: Antibodies against GLUR2/3 are implicated in autoimmune encephalitis, where they disrupt synaptic function and receptor clustering .
Phylogenetic Analyses: GLUR2/3 homologs (e.g., AtGLR2/3 in Arabidopsis) highlight conserved glutamate receptor evolution across species .
Western Blot: Optimal dilutions (e.g., 1:1,000 for NBP3-32478) and blocking agents (5% NFDM/TBST) are critical for reducing background .
Immunoprecipitation: Polyclonal antibodies (e.g., 07-598) show higher efficiency in IP due to broader epitope coverage .