Synaptic plasticity, the variable efficacy of neurotransmission at synapses, is thought to form the memories. Glutaminergic synapses mediate virtually all excitatory neurotransmission in mammalian brains. Glutamate released from presynaptic terminals activates several types of glutamate-gated ion channels on postsynaptic membranes, including a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, consist of subunits GluR1-GluR4, and N-methyl-D-aspartate (NMDA) receptors. Changes in AMPA receptors at the postsynaptic membrane cause changes in synaptic strength, the best-characterized forms of which are long-term potentiation (LTP) and long-term depression (LTD).

This antibody panel could be used to investigate the ratio of NMDAR to AMPAR or the change of AMPAR on the postsynaptic membrane. During the LTP, the AMPARs increase expression on the membrane of post-synapse, and the ratio of NMDAR to AMPAR would be higher than the pre-LTP. In construct, LTD decreases the AMPARs expression, and the ratio would be lower than pre-LTD.