Fig. 5

CX3CL1^-/- mice show deficits in LTP that are mitigated by treatment with mFKN and sFKN. a LTP was induced in hippocampal slices by high frequency stimulation (2 train, 4 Pulse, 1 s, 100 Hz bursts separated by 20 s with intertrain interval of 10s) following baseline recordings conducted over a period of 20 min. Changes in fEPSP slope were then monitored for a duration of 60 min and expressed as a percent of baseline. In comparison to WT controls, CX3CL1^−/− animals treated with AAV expressing GFP demonstrated significantly impaired potentiation that decayed over time to baseline levels. In contrast, treatment with either mFKN or sFKN partially preserved LTP in comparison to mice treated with GFP (n = 14). b Representative single signal of CX3CL1^−/− mice treated with mFKN showing instability in maintaining the LTP post theta burst stimulation. c Mean slope of the fEPSP was calculated for the last 20 min of the monitoring period, confirming that CX3CL1^−/− mice treated with GFP show significant deficits in LTP that are partially, but significantly ameliorated by treatment with either mFKN or sFKN. Data were analyzed by one-way ANOVA (n = 11, F (1.5, 15.03) = 1696, p < 0.0001) with Tukey’s test. ***p < 0.001. d The input/output curve for CX3CL1^−/− mice treated with sFKN were closer together with WT mice, whereas CX3CL1^−/− mice treated with mFKN were closer together with CX3CL1^−/− mice treated with GFP. Slopes are significantly different as determined by linear regression (n = 30, F (3, 112) = 170, p < 0.0001) suggesting that the presynaptic input and the post synaptic outpour for CX3CL1^−/− mice treated with GFP and mFKN were different from that of WT and CX3CL1^−/− mice treated with sFKN