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. 2020 Mar 19;11:1453. doi: 10.1038/s41467-020-15277-x

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© The Author(s) 2020

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. 4 — a Slice image and schematics (left) illustrating 2 × 4 octode probe placement and position of fibre-optic delivered light flash. Right panel shows the percentage of identified cells displaying suppressions or slow-activation following 10 ms light flashes (in total n = 37 and 3 cells respectively from 561 isolated neurons), from ex vivo recordings across the SPZ, PVN and ventral thalamus of VIP-ChR2 mice. b Peri-event spike raster plots for representative VIPⁱⁿ (supressed) and cells with slow-activation prior-to and following BIC application and subsequent co-application with VIP antagonist. c Mean ± SEM optogenetically-evoked change in firing rate of individual cells prior to and following antagonist treatment (n = 18 VIPⁱⁿ and n = 3 cells with slow-activation). Data analysed by multilevel mixed-effects linear model (Treatment: F_2,24.521 = 8.44, P = 0.002) with Tukey’s post-tests. d, e Pseudo-coloured spike raster for representative VIPⁱⁿ cell (d) and mean ± SEM baseline-subtracted firing rates across the population (e; n = 12 cells) during exposure to repeated stimulation (10 ms flashes) at varying frequencies, prior to and following antagonist treatment as above. f Mean ± SEM normalised change in firing (relative to no stimulation) for VIPⁱⁿ cells (n = 12) as a function of optogenetic stimulation frequency during pre-drug and antagonist treatment conditions. Data analysed by multilevel mixed-effects linear model (Frequency: F_5,21.785 = 6.99, P < 0.001; Treatment: F_2,20.357 = 49.72, P < 0.001; Interaction: F_10,23.401 = 16.71, P < 0.001) with Sidak’s post-test. ***P < 0.001, **P < 0.01.