Brain, behavior, and immunity · 2025
Effects of vagus nerve stimulation on microglia inhibit heroin-induced conditional place preference.
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Bai Jianhua, Yue Yingbiao, Zhang Zunyue, Wang Kunhua, Jin Yun, Wang Junfeng, Zou Lei
Аннотация
BACKGROUND: Heroin addiction remains a significant global health challenge with limited effective treatments. Vagus nerve stimulation (VNS) has shown promise in treating various neurological disorders, but its potential in addiction treatment is unexplored.
OBJECTIVE: To investigate the effects of VNS on heroin-induced conditioned place preference (CPP) and elucidate the underlying neurobiological mechanisms.
METHODS: We employed bilateral subphrenic vagotomy and VNS models in mice. Heroin-induced CPP was assessed following transcervical (nVNS) or transcutaneous auricular (taVNS) stimulation. Microglial activation in the nucleus accumbens (NAc) was evaluated using immunofluorescence and ELISA. The role of α7 nicotinic acetylcholine receptors (α7nAChRs) was investigated using the antagonist methyllycaconitine.
RESULTS: Both nVNS and taVNS significantly attenuated heroin-induced CPP. VNS reversed heroin-induced microglial activation in the NAc, reducing pro-inflammatory markers and cytokines while increasing anti-inflammatory markers. These effects were mediated by α7nAChRs, as antagonist administration abolished VNS efficacy. Notably, subphrenic vagotomy did not affect VNS efficacy, suggesting a primarily central mechanism of action.
CONCLUSION: VNS inhibits heroin-induced CPP, likely through modulation of NAc microglia via α7nAChRs. taVNS, while less effective than nVNS, offers a promising non-invasive approach to addiction treatment. These findings provide a rationale for further clinical investigation of VNS, particularly taVNS, as an adjunct therapy for heroin addiction.
BRIEF ABSTRACT: Vagus nerve stimulation (VNS) attenuates heroin-induced conditioned place preference in mice by modulating microglial activation in the nucleus accumbens via α7 nicotinic acetylcholine receptors. Both invasive and non-invasive VNS show efficacy, with the latter offering potential as a novel addiction treatment approach. These findings warrant further investigation of VNS in clinical settings for heroin addiction management.
OBJECTIVE: To investigate the effects of VNS on heroin-induced conditioned place preference (CPP) and elucidate the underlying neurobiological mechanisms.
METHODS: We employed bilateral subphrenic vagotomy and VNS models in mice. Heroin-induced CPP was assessed following transcervical (nVNS) or transcutaneous auricular (taVNS) stimulation. Microglial activation in the nucleus accumbens (NAc) was evaluated using immunofluorescence and ELISA. The role of α7 nicotinic acetylcholine receptors (α7nAChRs) was investigated using the antagonist methyllycaconitine.
RESULTS: Both nVNS and taVNS significantly attenuated heroin-induced CPP. VNS reversed heroin-induced microglial activation in the NAc, reducing pro-inflammatory markers and cytokines while increasing anti-inflammatory markers. These effects were mediated by α7nAChRs, as antagonist administration abolished VNS efficacy. Notably, subphrenic vagotomy did not affect VNS efficacy, suggesting a primarily central mechanism of action.
CONCLUSION: VNS inhibits heroin-induced CPP, likely through modulation of NAc microglia via α7nAChRs. taVNS, while less effective than nVNS, offers a promising non-invasive approach to addiction treatment. These findings provide a rationale for further clinical investigation of VNS, particularly taVNS, as an adjunct therapy for heroin addiction.
BRIEF ABSTRACT: Vagus nerve stimulation (VNS) attenuates heroin-induced conditioned place preference in mice by modulating microglial activation in the nucleus accumbens via α7 nicotinic acetylcholine receptors. Both invasive and non-invasive VNS show efficacy, with the latter offering potential as a novel addiction treatment approach. These findings warrant further investigation of VNS in clinical settings for heroin addiction management.