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. 2017 Jul 25;7(7):e1179. doi: 10.1038/tp.2017.144

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Copyright © 2017 The Author(s)

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

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Increased acetylcholine-evoked calcium signal in neuronal cells differentiated from KS-ASD patient-derived hiPSCs. (a) Expression of Nicotinic Acetylcholine Receptor beta 2 (AChRB2, green) in MAP2-positive 4-week-old hiPSC-derived nerurons. Scale bar=20 μm. (b) Change in fluorescence intensity upon administration of glutamate (Glu) or acetylcholine (ACh) onto 8-week-old control (CTL1) and KS-ASD neurons pre-loaded with Calcium 6-QF dye. Scale bar=50 μm. (c) Representative graphs showing Glu and ACh-evoked Ca-transients in CTL1 and KS-ASD neurons. Right panels, quantification of the Ca²⁺-responses as the mean of maximal intensity of the responses after treating the cells with Glu (upper) or ACh (lower). t-test, *P<0.05. KS-ASD, Autism spectrum disorder patient with Kleefstra syndrome.