There are phosphorylation sites within the C terminal domain of glutamate receptors(GluRs) which not only can be phosphorylated by protein kinases but can be dephosphorylated by protein phosphatases also. The effects of phosphorylation can enhance Ca²⁺ influx and improve the function of GluRs, whereas dephosphorylation do on the contrary. The reversible phosphorylation of GluRs keep balance in normal conditions which play an important role in synaptic plasticity such as LTP, but it can enhance excitatory neuronal damage in pathological events such as ischemic brain damage when the balance lose.