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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. 9 — SCFA treatment restored synaptic deficits in hippocampal CA1 neurons in cognitively compromised pain rats. A–C Effect of the SCFA intervention on the spontaneous synaptic transmission of excitatory neurons in hippocampal CA1 slices neurons. A Current-clamp recordings to identify excitatory neurons in the hippocampal CA1. B Representative mEPSC recording traces from the six groups. C Bar graphs showing the frequency and the amplitude of mEPSCs in hippocampal CA1 excitatory neurons. N = 5 rats for each group. D–F Effect of the SCFA intervention on the spontaneous synaptic transmission of hippocampal CA1 inhibitory neurons. D Current-clamp recordings to identify inhibitory neurons in the hippocampal CA1. E Representative mEPSCs of inhibitory neurons recording traces from the six groups. F Bar graphs showing the frequency and the amplitude of mEPSCs in hippocampal CA1 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