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. 2022 Aug 18;19:57. doi: 10.1186/s12989-022-00497-4

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Effect of temperature on burst frequency of the respiratory CPG in unexposed and prenatally TiO₂ NP-exposed neonates. A Schematic of experimental procedure. B Raw extracellular burst activity recorded from a C4 ventral root in isolated preparations from unexposed (Control, green traces) and prenatally TiO₂ NP (200 µg/g)-exposed (purple traces) neonates under standard (24 °C, upper traces) and elevated (29 °C, lower traces) bath temperatures. C Bar charts showing changes in spontaneous respiratory burst frequency as a function of time (mean ± SEM) in control (green bars) and prenatally TiO₂ NP-exposed (purple bars) groups under the warming protocol. Data were pooled from P0 to P3. *p < 0.05; ns, not statistically significant