Figure 3

IFN-β reduced I _M and accordingly attenuated amplitudes of after-hyperpolarizations, as did pharmacological protein kinase C activation in layer 5 pyramidal neurons on neocortical ex vivo rat slices under whole-cell recording conditions. (A) Voltage-clamp recordings of I _M tail currents depicted at the deactivating voltage of -50 mV following a 30-second depolarization to -30 mV (top) in a layer 5 pyramidal neuron before (black trace) and during (green trace) application of 1,000 IU ml^-1 IFN-β. Population data of IFN-β-mediated reduction of I _M (bottom). (B-D) Current-clamp recordings reveal after-hyperpolarizations (AHP) following a train of action potentials at similar suprathreshold depolarization (top) without (black traces) and with activation of protein kinase C (PKC) by 1,000 IU ml^-1 IFN-β (B), 1 μM 4β-phorbol 12-myristate 13-acetate (4β-PMA) (C), and 1 μM Bryostatin1 (D) (green traces). We estimated AHP amplitudes as difference between the steady state of tail current and the largest hyperpolarization of AHP. Population data show a consistent reduction under all PKC activating conditions (bottom). *P < 0.05, **P < 0.01, ***P < 0.005. ctrl, Control.