# Low-frequency electroacupuncture attenuates methamphetamine-induced depressive-like behaviors and cognitive impairment via modulating neuroinflammation

## TL;DR

Low-frequency electroacupuncture reduces depression-like behaviors and cognitive issues caused by methamphetamine by reducing brain inflammation.

## Contribution

This study demonstrates that low-frequency electroacupuncture can alleviate methamphetamine-induced neuroinflammation and cognitive deficits in mice.

## Key findings

- Low-frequency EA significantly reduced depressive-like behaviors and cognitive impairment in mice.
- EA restored blood-brain barrier integrity and reduced neuronal injury.
- EA suppressed microglial activation and pro-inflammatory cytokines like IL-6 and TNF-α.

## Abstract

Methamphetamine (METH) abuse primarily affects the central nervous system (CNS), leading to CNS damage and contributing to depressive-like behaviors, cognitive impairment, and other neuropsychiatric disorders. Electroacupuncture (EA) has shown promise in treating mental disorders linked to CNS damage, yet the effects of EA on METH-induced depressive-like behaviors and cognitive impairment and it’s underlying therapeutic mechanisms remain largely unclear.

In this study, a mouse model of METH-induced neuropsychiatric dysfunction was established by administering high-dose METH under elevated ambient temperature. EA was applied at different frequencies to the Zusanli (ST36) acupoint for 7 days post-METH administration.

Behavioral tests revealed that low-frequency EA significantly alleviated depressive-like behaviors and cognitive impairment. Additionally, EA restored blood-brain barrier (BBB) integrity, as evidenced by Western blotting (WB) and Evans blue staining. Neuronal injury was attenuated, as shown by Nissl and hematoxylin and eosin (HE) staining. Further investigations into neuroinflammation revealed that EA suppressed microglial activation in the hippocampus, decreased the expression of IL-6 and TNF-α, and inhibited the NF-κB/NLRP3 signaling pathway.

The present study suggested that EA alleviates METH-induced depressive-like behaviors and cognitive impairment by modulating neuroinflammation, particularly through the inhibition of microglial activation and pro-inflammatory cytokine release. EA may represent a promising non-pharmacological strategy for the treatment of METH-associated neuropsychiatric disorders.