PTGER1 and brain injury: Various biological actions of the specific prostaglandins are mediated via activation of several different isotypes of their cognate membrane G-protein-coupled receptors (GPCRs), and thus far the data suggest that the prostaglandin receptors, which exert most of their action through activation of intracellular calcium (Ca2+)-signaling, such as closely related PGE2 receptor EP1 and PGF2α receptor FP [11], [17]–[19], exacerbate neuronal dysfunction after ischemic and excitotoxic brain injuries [11], [17], [19]–[23].