Acupuncture anesthesia

Evidence Details for Syn2

PMID	Title	Journal	Year	Abstract
36440366	Electroacupuncture Activates Neuroplasticity in the Motor Cortex and Corticospinal Tract via the mTOR Pathway in a Rat P-MCAO Model.	Biomed Res Int. 2022 Nov 14;2022:3470685. doi: 10.1155/2022/3470685. eCollection 2022.	2022	Electroacupuncture (EA) combines traditional Chinese medicine acupuncture theory with modern scientific technology. It is a promising therapy for the treatment of cerebrovascular diseases such as cerebral infarction. A large number of clinical studies have shown that EA promotes recovery of neurological function after cerebral infarction, however, the underlying mechanisms behind its effects remain unclear. We tested whether EA stimulation of the Zusanli (ST36) and Neiguan (PC6) acupoints activates neuroplasticity in rats with ischemic stroke and whether this involves the regulation of axonal regeneration through the mTOR pathway. 24 h after permanent middle cerebral artery occlusion (p-MCAO) in rats, EA treatment was started for 20 min, daily, for 14 days. We found that EA significantly reduced Modified Neurological Severity Scores (mNSS), cerebral infarct volume, and apoptosis of neuronal cells. EA also significantly increased the expression of the neuroplasticity-associated proteins GAP-43 and SYN and upregulated the phosphorylation levels of AKT, mTOR, S6, and PTEN to promote CST axon sprouting in the spinal cord at C1-C4 levels. The positive effects of EA were blocked by the administration of the mTOR inhibitor Rapamycin. In short, we found that EA of the Zusanli (ST36) and Neiguan (PC6) acupoints in p-MCAO rats induced neuroprotective and neuroplastic effects by regulating the mTOR signaling pathway. It promoted neuroplasticity activated by axon regeneration in the contralateral cortex and corticospinal tract. Activation of such endogenous remodeling is conducive to neurological recovery and may help explain the positive clinical effects seen in patients with infarcts."

Evidence Sentence:	EA also significantly increased the expression of the neuroplasticity-associated proteins GAP-43 and SYN and upregulated the phosphorylation levels of AKT, mTOR, S6, and PTEN to promote CST axon sprouting in the spinal cord at C1-C4 levels.
Evidence Sentence:	We used Western blotting to detect neuroplasticity-related proteins, including GAP-43 and SYN (Figure 2(b)).
Evidence Sentence:	As shown in Figure 2(e), SYN expression was significantly increased in the EA group compared with the p-MCAO group (p < 0.01); this positive effect was counteracted by rapamycin and the expression of SYN was significantly lower in the EA + R group compared with the EA group (p < 0.01).
Evidence Sentence:	These results show that EA after p-MCAO increases the expression of GAP-43 and SYN in the contralateral cerebral cortex, suggesting that EA intervention after p-MCAO can help drive motor function recovery by enhancing neuroplasticity.
Evidence Sentence:	To further confirm the relationship between neuroplasticity-related proteins and the mTOR pathway, we detected the expression of SYN and p-S6 by immunofluorescence (Figures 3(a) and 4(a)).
Evidence Sentence:	As shown in Figure 3(b), SYN expression was significantly increased in the p-MCAO group compared with the Sham group (p < 0.05), SYN was more increased in the EA group compared with the p-MCAO group (p < 0.001), lower in the p-MCAO + R than the p-MCAO group (p < 0.01), and lower in the E + R than the EA group (p < 0.001).
Evidence Sentence:	Double immunofluorescence showed that p-S6 was present around SYN in the healthy cerebral cortex; these markers were even found to be coexpressed.
Evidence Sentence:	Such SYN+/p-S6+ coexpressing cells were significantly increased after EA (Figure 5).
Evidence Sentence:	This suggests that SYN correlates with p-S6 and that EA can modulate neuroplasticity through the mTOR pathway.
Evidence Sentence:	In addition, we found that SYN and p-S6 were expressed around BDA markers; EA significantly increased the expression of BDA+/SYN+ and BDA+/p-S6+ positive cells (Figures 8 and 9), demonstrating that EA promotes SYN expression and activates CST axon germination in the cervical medullary gray matter via the mTOR pathway.