Skip to main content
. 2015 Jul 15;112(30):E4129–E4137. doi: 10.1073/pnas.1511910112

Fig. 1.

Fig. 1.

Loss of LGI1 reduces synaptic, but not surface, AMPAR content. (A) Timeline of experimental preparation for hippocampal slice cultures and recordings (Bottom) compared with the LGI1−/− phenotype (Top). (B) AMPA/NMDA ratios recorded in slice cultures made from LGI1−/− mice are significantly reduced (P = 0.03, n = 15) compared with wild type. (Left) Sample traces of wild type (black) and LGI1−/− (gray). (Scale bar, 50 ms and 50 pA.) (Right) Bar graphs showing average AMPA/NMDA ratios ± SEM in wild type and LGI1−/−. (C) Paired-pulse stimulation reveals no significant difference (P = 0.46, n = 16 wild type, 17 LGI1−/−) in presynaptic release probability in LGI1−/− relative to wild type. (Left) Sample traces normalized to first-response amplitude in wild-type cell. (Scale bar, 40 ms.) (Right) Average ratio ± SEM (D) Miniature EPSC recordings in wild type and LGI1−/−. Loss of LGI1 results in a significant decrease in amplitude (P = 0.03, n = 21), but not frequency (P = 0.17, n = 21), of mEPSCs. Bar graphs of average amplitude and frequency of mEPSCs ± SEM, with sample traces for each condition shown above. [Scale bars, 25 ms (amplitude traces), 100 ms (frequency traces), and 10 pA.] (E) Somatic outside-out patch recordings in wild-type and LGI1−/− cells have similar glutamate-evoked currents (P = 0.92, n = 13). (Top) Sample traces of wild-type and LGI1−/− surface currents. (Scale bars, 1 s and 100 pA.) (Bottom) Average glutamate-evoked currents ± SEM.