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. 2017 Nov 27;8:1791. doi: 10.1038/s41467-017-01700-3

Fig. 7.

Fig. 7

NMDAR-Ab from Healthy + subjects and PSY + patients do not affect NMDAR-mediated Ca2+ transients in spines of hippocampal neurons. a Representative time-lapse images of a spontaneous NMDAR-mediated Ca2+ transient in basal condition (in the presence of nifedipine 5 µM and bicuculline 5 µM). Scale bar, 2 µm. Lower panel, representative examples of NMDAR-mediated Ca2+ transients recorded in spines (expressed as ΔF/F ratio) exposed to purified IgG from Healthy −, Healthy +, or PSY + individuals. Note that all events were abolished by the NMDAR-competitive antagonist D-AP5 (50 µM). b Normalized frequency (ratio of Ca2+ transients frequency post-application of NMDAR-Ab relative to the baseline acquisition) of spontaneous NMDAR-mediated Ca2+ transients in control condition with no IgG (n = 38 spines, N = 4 neurons) or in the presence of Healthy − purified IgG (n = 38, N = 5), Healthy + NMDAR-Ab (n = 68, N = 10), or PSY + NMDAR-Ab (n = 131, N = 15). Data are expressed as mean ± SEM. One out of one Healthy − , three out of three Healthy + , and four out of nine PSY + were used and pooled for comparisons. P > 0.05, Krukal–Wallis test