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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. 5 — A hypothetical mechanism for SCFAs alleviates pain-related cognitive deficits by improving histone acetylation and synaptic transmission. The gut microbiota metabolites (acetate and butyrate) approach brain tissue by blood flow and reduce permeability to the gut and BBB (blood–brain barrier). In the nucleus, this acetate was converted into acetyl-CoA by ACSS2 (acetyl-CoA synthetase2) to supply carbon for histone acetylation. Butyrate, an HDAC inhibitor, inhibits histone deacetylase activity to increase histone acetylation. Improved histone acetylation restores the excitatory synaptic input to the excitatory and inhibitory neurons in the mPFC, CeA, and hippocampal CA1 areas in the synapses. Then, improved histone acetylation and synaptic transmission alleviate pain-related cognitive deficits