Fig. 1

TNF-α induces hyperexcitability of RGCs through activating TNFR1. a Representative traces show spontaneous firing and evoked action potentials (AP) that were recorded in three different RGCs in rat retinal slices obtained from control (Ctr), 3 days (TNF-α3D) and 7 days (TNF-α7D) after intravitreal TNF-α injections. (a1) and (a2) are those from the recordings in a in a faster time scale. b, c Summary data show the changes in frequency (b) and membrane potential (MP) (c) of spontaneous firing in RGCs under different conditions. d Summary data show the changes in the frequency of spontaneous firing in RGCs under different conditions when synaptic transmissions were blocked. The insert shows the percentage of AP firing cells in different groups. e Summary data show the changes in the frequency of evoked AP under different conditions. n = 11 for each group. f–h Representative traces show spontaneous firing that was recorded in three different RGCs in rat retinal slices obtained from Ctr, TNF-α7D, and R7050+TNF-α7D groups, respectively. i Summary data show that the TNFR1 inhibitor R7050 eliminated TNF-α-induced increase of spontaneous firing frequency. n = 12, 11, 14, respectively. Data are represented as median and interquartile range. *P < 0.05, **P < 0.01, and ***P < 0.001 vs. Ctr; ^###P < 0.001 vs. TNF-α7D