Figure 3
CSF from NMDAR-Ab encephalitis patients contains neuronal antibodies and does not increase ivNNA in comparison to aCSF. (A) To verify the presence of neuronal antibodies in CSF from NMDAR-Ab or LGI1-Ab patients, we applied pCSF and hCSF samples on non-permeabilized dissociated primary mouse hippocampal neurons (10 days in vitro, βtubulin, TuJ1, immunocytochemistry, red) that are known to express NMDARs containing the target antigens. Indeed, pCSFNMDAR and pCSFLGI1 showed a strong immunoreactivity (green) with overlap on neurons (merged photomicrograph, yellow), while control samples (hCSF) did not. In (B–D) ratios of absolute values for spikes/minute, bursts/minute and PFR are given. We calculated the respective values for human CSF (either hCSF from controls, n = 13; pCSFLGI1, n = 6; or pCSFNMDAR, n = 7) divided by those for aCSF: pCSF-LGI1, for instance, shows the value pCSFLGI1/aCSF. Shown are all individual samples as dots, the mean value as bar graph, and error bars represent S.E.M. In (E–G) spike raster plots (SRPs) are illustrated, visualizing the decreased activity under the influence of pCSFNMDAR (G) or pCSFLGI1 (F) compared to hCSF (E).
