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. 2021 Feb 19;11:136. doi: 10.1038/s41398-021-01262-5

Fig. 2. ZIP8 total knockout (KO) and loss-of-function allele A391T displays neuronal activity-dependent deficits in glutamate receptor-mediated sEPSCs.

Fig. 2

A, B Quantification of sEPSC amplitude (A) and frequency (B) recorded from cultured D28-30 neurons. *P < 0.05 (Student’s t-test, n = 6–10 per group). Error bars, SEM. C Representative raw traces of glutamate receptor-mediated sEPSCs in cultured pyramidal neurons expressing either Luc-shRNA, Zip8-shRNA, Zip8-shRNA + ZIP8WT plasmid, or Zip8-shRNA + ZIP8A391T plasmid. Note the significant loss of sEPSC amplitude, not frequency, in the presence of the ZIP8A391T mutation, consistent with the loss-of-function observed in Fig. 1. No changes were observed in mEPSC amplitude or frequency (Fig. S1).