During prolonged pathophysiological conditions, including traumatic brain injury and ischemia, prolonged and sustained activation of NMDARs will likely cause the activation of the phosphatase PP2A (Terunuma et al., 2010), leading to dephosphorylation of S783, decreasing the number of surface GABABRs by increasing internalization and degradation. The gene discussed is PTPA; the disease is ischemia.