The lack of effects of the EP1 receptor pharmacological blockade or knockout on either neurobehavioral and anatomical outcomes or Iba1 and GFAP immunohistochemistry in our in vivo CCI model of TBI, which is in contrast with the neuroprotective effects observed in the related in vitro studies [18], [34] and the in vivo models of ischemia and excitotoxicity [19], [22], [23], [40], suggests that involvement of other cell types expressing the EP1 receptor contribute considerably to the brain pathology following TBI. Here, GFAP is linked to ischemia.