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. 2020 Jan 10;11:221. doi: 10.1038/s41467-019-13938-0

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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 Top: Example of call-related bursting for a premotor neuron recorded during saline control. Bottom: Same cell as (top) but recorded during local gabazine infusion. x, y scale bars: 10 ms, 10 mV. b Number of call-related spikes per burst in premotor neurons recorded under control or gabazine conditions (control: 2.4 ± 1.2 spikes per burst, n = 14 neurons in 10 birds, 2 were active during both call types; gabazine: 5.7 ± 2.8 spikes per burst, Wilcoxon rank-sum test, p = 0.003, n = 9 neurons in 3 birds). c Mean burst onset latency relative to call onsets for premotor neurons recorded during control conditions (blue) vs. premotor neurons recorded during gabazine microinfusion (orange), (spiking onset for control: −10 ± 22 ms, n = 14 neurons, for gabazine: −26 ± 26 ms, Wilcoxon rank-sum test, p = 0.039, n = 9 neurons). Source data is available as a Source Data file.