The results of this study highlight some important facts: (i) in early and late sepsis, the IRP component of LTP in fEPSPs was initially suppressed or reduced, then the LTP developed gradually; (ii) in late sepsis, LTP in PSs was strongly potentiated, and its peak was delayed; and (iii) the late sepsis-induced potentiation of LTP in PSs was depressed by SOD. The gene discussed is SOD1; the disease is Sepsis.