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. 2018 Aug 21;9:3339. doi: 10.1038/s41467-018-05847-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Selective modulation of cortically-evoked spiking activity by SOM and PV cells. a Experimental set up: electrical stimulations were applied in the cortex and evoked APs were recorded in SPNs, in control or with specific opto-inhibition of PV cells or SOM cells in transgenic mice PV::Arch3 and SOM::Arch3 (top) or PV-Cre and SOM-Cre mice virally infected with AAV-Flex-Arch-tdtomato (bottom) (Arch3 activation for 300 ms with a 570 nm LED). b, c The spiking probability of SPNs was compared between interleaved control and opto-inhibition conditions in DMS (b) and DLS (c) using transgenic mice (top, black) or virally infected interneurons (bottom). Individual experiments and averaged (mean ± SEM) normalized spiking probability are represented. Opto-inhibition of SOM cells leads to a significant increase in spiking probability in DMS (n = 15, p = 0.0063 for transgenic and n = 8, p = 0.033 for virus experiments) and no difference in DLS (n = 10, p = 0.2567 for transgenic and n = 6, p = 0.55479 for viruses). For PV cells, the effect is opposite, opto-inhibition of PV cells significantly increase the spiking probability in DLS (n = 16, p = 0.0288 for transgenic and n = 5, p = 0.0063 for viruses), while their opto-inhibition has no effect in DMS (n = 7, p = 0.1854 for transgenic and n = 9, p = 0.8007 for viruses). d Experimental set up: electrical stimulations were applied in the cortex and evoked APs were recorded in SPNs, in control or with specific opto-activation of PV cells or SOM cells with ChR2 activation in transgenic mice PV::ChR2 and SOM::ChR2 (top) or PV-Cre and SOM-Cre mice virally infected with AAV-Flex-ChR-mCherry (bottom) (for 5 ms using a 470 nm excitation LED). e, f The spiking probability of SPNs was compared between the control and opto-activation conditions in DMS (e) and DLS (f) using transgenic mice (top, black) or virally infected interneurons (bottom, red). Individual experiments and averaged normalized spiking probability are represented. SOM opto-activation leads to a significant decrease in spiking probability in DMS (n = 7, p = 0.0002 for transgenic mice and n = 7, p = 0.0002 for viral experiments) and no difference in DLS (n = 6, p = 0.9114 for transgenic and n = 5, p = 0.9980 for viruses). Opto-activation of PV cells significantly decrease the spiking probability in DLS (n = 9, p = 0.0059 for transgenic and n = 7, p = 0.0023 for viruses) but not in DMS (n = 9, p = 0.9816 for transgenic and n = 6, p = 0.4518 for viruses). Paired tests, *p < 0.05, **p < 0.01, ***p < 0.001