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. 2012 Aug 8;32(32):11082–11094. doi: 10.1523/JNEUROSCI.0064-12.2012

Figure 1.

Figure 1.

Patients' antibodies recognize the ATD of GluN1 and are not dependent on splice variant or GluN2 domains. A, Patients' antibodies (pt CSF) recognize both splice variants that lack (GluN1a) and include (GluN1b) exon 5 (GluN1a = 0.482 ± 0.088 AU; GluN1b = 0.586 ± 0.073 AU (where AU is arbitrary units); n = 5 patients, p > 0.05, t test with Welch's correction). CSF from individuals without anti-NMDAR encephalitis (con CSF) does not stain GluN1-transfected HEK cells. B, Antibody staining is not affected by the absence of domains within GluN2B (n = 7 patients, p > 0.05, one-way ANOVA plus Tukey's post hoc testing). C, The ATD of GluN1 is both necessary and sufficient for staining by patients' antibodies, although the lack of other extracellular and transmembrane domains does decrease antibody staining (n = 7–10 patients, **p < 0.01, ***p < 0.001, one-way ANOVA plus Tukey's post hoc testing).