Electroacupuncture Activates Neuroplasticity in the Motor Cortex and Corticospinal Tract via the mTOR Pathway in a Rat P-MCAO Model

BioMed Research International, 2022 · DOI: https://doi.org/10.1155/2022/3470685 · Published: November 14, 2022

Alternative Medicine Neurology Neuroplasticity

Simple Explanation

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. This study investigated whether electroacupuncture stimulation of specific acupoints regulates axonal regeneration after ischemic brain injury through the mTOR signaling pathway, and activates neuroplasticity to achieve neuroprotective effects. The study found that electroacupuncture induced neuroprotective and neuroplastic effects by regulating the mTOR signaling pathway, promoting neuroplasticity activated by axon regeneration in the contralateral cortex and corticospinal tract.

Study Duration

14 days

Participants

100 male Sprague Dawley (SD) rats

Evidence Level

Not specified

Key Findings

1
EA significantly reduced Modified Neurological Severity Scores (mNSS), cerebral infarct volume, and apoptosis of neuronal cells in rats with permanent middle cerebral artery occlusion (p-MCAO).
2
EA increased the expression of neuroplasticity-associated proteins GAP-43 and SYN and upregulated the phosphorylation levels of AKT, mTOR, S6, and PTEN to promote CST axon sprouting.
3
The positive effects of EA were blocked by the administration of the mTOR inhibitor Rapamycin, suggesting the involvement of the mTOR pathway in EA's neuroprotective and neuroplastic effects.

Research Summary

This study demonstrates that electroacupuncture (EA) can significantly improve neurological deficits, reduce cerebral infarct volume, and decrease neuronal damage in a rat model of ischemic stroke (p-MCAO). EA promotes neuroplasticity by increasing the expression of GAP-43 and SYN, and modulates the mTOR pathway by upregulating the phosphorylation levels of AKT, mTOR, S6, and PTEN. The neuroprotective and neuroplastic effects of EA are dependent on the mTOR pathway, as evidenced by the reversal of these effects with the mTOR inhibitor rapamycin, suggesting that EA's benefits are mediated through mTOR signaling.

Practical Implications

Therapeutic Potential

EA could be a promising therapy for stroke rehabilitation by promoting neuroplasticity and reducing brain damage.

Targeted Intervention

EA's effects on the mTOR pathway provide a potential target for enhancing stroke recovery.

Clinical Application

The study supports the clinical use of EA in stroke patients to improve neurological function and quality of life.

Study Limitations

1
The study was conducted on rats, and the results may not be directly applicable to humans.
2
The specific mechanisms by which EA activates the mTOR pathway and regulates GAP-43 and SYN require further investigation.
3
The long-term effects of EA on neuroplasticity and functional recovery after stroke were not assessed.

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