Journal: eLife

Article Title: CNTN5 - /+ or EHMT2 - /+ human iPSC-derived neurons from individuals with autism develop hyperactive neuronal networks

doi: 10.7554/eLife.40092

Figure Lengend Snippet: ( A ) Representative trace of the amplitude of an action potential during time, detected by one electrode from one well populated with line 37E. ( B ) MEA recordings of the MFR and number of network bursts of different iPSC-derived neuronal lines upon treatments with different receptor inhibitors. Values were acquired in four consecutive readings, that is, before (read 1) and after addition of GABA receptor inhibitor PTX (read 2), after addition of AMPA receptor inhibitor CNQX (read 3), and after addition of sodium channel blocker TTX (read 4). At least 60 min recovery was allowed after each reading, which were performed 5–10 min after treatment with neurotoxins. 6–8 wells were recorded for each group at week 8 PNI. Values are presented as mean ± SD from a single experiment; *p<0.05 between n/t and CNQX for all samples; PTX, Picrotoxin; CNQX, 6-Cyano-7-nitroquinoxaline-2,3-dione; TTX, Tetrodotoxin; n/t, not treated; μV, microvolt; Hz, hertz; ctrl, control; mut, mutant.

Article Snippet: After the last reading, each well was treated with three synaptic antagonists: GABA A receptor antagonist picrotoxin (PTX; Sigma) at 100 μM, AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dion (CNQX; Sigma) at 60 μM, and sodium ion channel antagonist tetrodotoxin (TTX; Alomone labs) at 1 μM.

Techniques: Derivative Assay, Mutagenesis