mTBI reduced the phosphorylation of ERK1/2 and CREB, key signaling molecules downstream of synaptic NMDAR activation, consistent with previous findings in chronic TBI models [67,68,69,70] and as shown in Figure 4I. Exo70 overexpression restored the phosphorylation of these proteins, further supporting the idea that it promotes functional synaptic NMDAR signaling. Here, EXOC7 is linked to concussion.