Fig. 7
Global depletion of IKKβ from myeloid cells results in exacerbated neuronal excitability in EAE. A Bipolar stimulating electrodes (St.) were chronically implanted in the CA3 area of the right hippocampus to activate the Schaffer collateral/commissural pathway (Schaffer coll.). Recording electrodes (Rec.) were implanted in the ipsilateral CA1 area. B Representation of the mean EAE clinical score for IKKβF/F and MφIKKβΚΟ male mice with implanted electrodes, over 25 days post immunization with the peptide MOG35-55. C Regression lines illustrating input/output curves evoked at the CA3–CA1 synapse of IKKβF/F (n = 6) and MφIKKβKO (n = 5) mice. Paired pulses (40 ms of interstimulus interval) were delivered at increasing intensities in 20 μA steps. At the right are illustrated representative examples of fEPSP recordings (evoked at 0.2, 0.3 and 0.4 mA) of IKKβF/F and MφIKKβΚΟ mice. D Regression lines illustrating input/output curves evoked at the CA3–CA1 synapse of IKKβF/F (n = 6) and mφIKKbKO (n = 5) mice under naïve conditions (before immunization—black) and during MOG35-55-induced EAE, specifically at a pre-onset stage (dpi 6—pink), at the onset (dpi 9—orange), at the peak (dpi 13—green) and at a chronic (dpi 21—blue) phase of the disease. Representative examples of fEPSP recordings (0.3 mA) of IKKβF/F and MφIKKβΚΟ mice are also illustrated. All mice in this graph were adult males, 3–5 months old