Glutamate / Excitotoxicity Antibody Sampler Pack

Glutamate / Excitotoxicity Antibody Sampler Pack

The Glutamate / Excitotoxicity Antibody Sampler Pack from Assay Genie brings together 8 rigorously validated antibodies spanning the key nodes of this pathway, supplied in a convenient 20µL trial size. It lets researchers screen an entire signalling axis in a single, cost-effective pack — validated for applications including ELISA, IF/ICC, IP, WB — before committing to full-size vials. Each antibody is also available individually in a full 100µL size.

Glutamate is the principal excitatory neurotransmitter of the central nervous system, and the same signaling that underlies synaptic plasticity becomes destructive when glutamate accumulates excessively, a process termed excitotoxicity that contributes to stroke, traumatic injury, epilepsy, and chronic neurodegeneration. Fast excitatory transmission and plasticity are mediated by ionotropic glutamate receptors. The NMDA receptor, an obligate heteromer, includes the essential subunit NMDAR1/GRIN1 together with regulatory subunits such as NMDAR2B/GRIN2B, which confers slow kinetics and high calcium permeability and is strongly implicated in excitotoxic calcium overload. AMPA receptors mediate the bulk of rapid depolarization, and their subunit GluA1/GRIA1 is dynamically trafficked to and from synapses during long-term potentiation. Metabotropic signaling through mGluR5/GRM5 couples glutamate to intracellular calcium release and modulates synaptic strength and excitability. A key decoder of the resulting calcium signals is CaMKII, a kinase that, upon autophosphorylation to Phospho-CaMKII, becomes persistently active and drives the synaptic changes that consolidate memory, while excessive activation participates in excitotoxic injury. The magnitude and duration of glutamate signaling are constrained by clearance and by inhibitory balance. EAAT2/GLT-1, the dominant astrocytic glutamate transporter, removes synaptic glutamate to terminate transmission and prevent toxic accumulation, and its dysfunction is a recognized contributor to excitotoxic disease. Inhibitory tone that opposes excitation depends on GABA synthesis by GAD67, the glutamate decarboxylase isoform that sets baseline GABA levels. Together these targets span receptor signaling, calcium decoding, transporter-mediated clearance, and excitatory-inhibitory balance. This pack brings together validated antibodies against NMDAR1/GRIN1, NMDAR2B/GRIN2B, GluA1/GRIA1, mGluR5/GRM5, CaMKII, Phospho-CaMKII, EAAT2/GLT-1, and GAD67 to support study of glutamatergic signaling and excitotoxicity.