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. 2022 Aug 9;16:880267. doi: 10.3389/fncel.2022.880267

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Copyright © 2022 Hung, Chung, Luo, Chu, Chen, MacDonald, Chien, Kotha, Yang, Hwang, Dun, Chuang and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A proposed working model depicting neurochemical, neurobiological, and behavioral changes after traumatic brain injury (TBI) and their reversal or protection by EA after the insult. TBI induces overexpression of certain HDAC isoforms, notably HDAC1 and HDAC3. The cell survival BDNF-associated Akt/GSK-3β signaling pathway is also downregulated after TBI; this could be directly mediated by the brain injury or indirectly mediated through overexpressed HDACs. Either the overexpression of HDACs or aberrant BDNF-associated Akt-GSK-3β signaling may lead to activation of microglia and astrocytes as well as increased expression of the proinflammatory cytokine TNF-α and IL-6. Either of these aberrant neurochemical events may also trigger overexpression of the proapoptotic factor Bax to induce neuronal apoptosis. The end result is marked deficits in motor and sensory behavioral performance as well as impaired learning and memory. EA treatment at the acupoints normalizes these neurobiological events and robustly facilitates behavioral recovery.