Figure 5
Blocking protein kinase C activation prevents IFN-β effects on excitability of neocortical layer 5 neurons in ex vivo whole-cell recordings. (A) Family of voltage traces from a layer 5 neuron recorded in current clamp mode compared with under control conditions (artificial cerebrospinal fluid, black traces, top) and following 30 minutes co-application of protein kinase C (PKC) inhibitor 1 μM GF109203X and 1,000 IU ml-1 IFN-β (green traces, middle) yield no obvious differences in firing behavior. The initial input resistance and capacitance of the depicted neuron were 132 MΩ and 130 pF, respectively. (B) Population data reveal similar input resistance (Rin), suggesting that PKC activation is necessary for subthreshold IFN-β effects. (C) Rate of action potentials of a layer 5 neuron plotted against the strength of rectangular current injections (left). Population data show that rheobase (middle) and F-I slope (right) remain comparable to control values when IFN-β was co-applied with GF109203X. (D) Example traces of a layer 5 neuron after pre-incubation with 100 nM calphostin C (black traces) and 20 minutes after application of IFN-β (1,000 IU ml-1) (green traces) revealed also no difference in firing behavior. The initial input resistance and capacitance of the depicted neuron were 158 MΩ and 157 pF, respectively. (E) Population data of Rin confirmed that PKC activation is needed for IFN-β effects. (F) Number of action potential plotted against the strength of rectangular current injection (left). Population data indicate no difference of rheobase (middle) or F-I slope (right) between pre-incubation of calphostin C and 20 minutes of IFN-β administration. ctrl, Control.