KCC2-GABAA pathway correlates with analgesic effect of electro-acupuncture in CCI rats

Molecular Medicine Reports, 2018 · DOI: 10.3892/mmr.2018.8766 · Published: May 8, 2018

Alternative Medicine Neurology Pain Management

Simple Explanation

This study investigates how electro-acupuncture (EA) affects neuropathic pain (NP) in rats. It looks at the levels of KCC2 and GABAA receptor γ2 subunit in the spinal cord. The study found that EA stimulation at specific acupoints improved mechanical withdrawal threshold and thermal withdrawal latency in rats with chronic constriction injury (CCI). EA treatment reversed the reduction in KCC2 and GABAA receptor γ2 subunit expression caused by CCI, suggesting these factors contribute to NP and that EA's analgesic effects involve these pathways.

Study Duration

Not specified

Participants

60 adult male Sprague‑Dawley rats

Evidence Level

Not specified

Key Findings

1
EA treatment significantly improved mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) in CCI model rats, indicating reduced pain.
2
CCI led to a marked reduction in both mRNA and protein levels of KCC2 and GABAA receptor γ2 subunit in the spinal cord.
3
EA treatment reversed the CCI-induced reductions in KCC2 and GABAA receptor γ2 subunit expression in the spinal cord.

Research Summary

The study demonstrated that EA treatment has a beneficial effect on the pain threshold of rats undergoing CCI, increasing mechanical and thermal nociceptive thresholds. EA treatment significantly increased KCC2 and GABAA receptor γ2 subunit expression in CCI rats, suggesting a link between these factors and EA's analgesic effect. The findings suggest that the mechanical allodynia and thermal hyperalgesia mediated by the KCC2‑GABAA receptor signaling pathway is attenuated by EA via its immunomodulatory effects in the spinal cord.

Practical Implications

Analgesic Effect Mechanism

The study suggests that the analgesic effect of EA in neuropathic pain may be mediated through the KCC2-GABAA receptor signaling pathway.

Therapeutic Intervention

EA may serve as a viable therapeutic intervention to alleviate chronic pain, particularly neuropathic pain, by modulating KCC2 and GABAA receptor γ2 subunit expression.

Drug Target

The KCC2-GABAA receptor pathway may be a potential drug target for the development of novel analgesics.

Study Limitations

1
The precise mechanisms underlying EA's immunomodulatory effects in the spinal cord require further investigation.
2
Further studies are needed to characterize the analgesic effect of EA using pharmacology, electrophysiological techniques, and other methods.
3
The study was conducted on rats, and further research is needed to confirm these findings in humans.

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