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. 2022 Jul 28;59(10):6211–6227. doi: 10.1007/s12035-022-02971-8

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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/.

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Fig. 7 — SCFA treatment rescued synaptic deficits in layer II/III of the mPFC neurons in cognitively compromised pain rats. A–C Effect of the SCFAs intervention on the spontaneous synaptic transmission of excitatory neurons in pain-induced cognitive deficits rats. A Current-clamp recordings to identify excitatory neurons in the mPFC slices. B Original traces of mEPSCs of excitatory neurons recorded from the six groups. C Bar graphs showing the frequency and the amplitude of mEPSCs in mPFC excitatory neurons. N = 5 rats for each group. D–F Spontaneous synaptic transmission of the mPFC inhibitory neurons in slices. D Current-clamp recordings to identify inhibitory neurons in the mPFC slices. E Original traces of mEPSCs in slices from the six groups. F Bar graphs showing the frequency and the amplitude of mEPSCs in mPFC inhibitory neurons. Results are expressed as mean ± SEM; n = 5 rats for each group. Tukey’s post hoc tests; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001