ArticleClinical and translational medicine2024
Corticostriatal glutamate-mediated dynamic therapeutic efficacy of electroacupuncture in a parkinsonian rat model.
Article in Clinical and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy of various acupuncture modalities on alleviating symptoms in Parkinson's disease: a systematic review and meta-analysis of randomized controlled trials.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Pooled it
- Efficacy of personalized acupuncture combined with accelerated deep transcranial magnetic stimulation in mild cognitive impairment: A randomized controlled trial.Integrative medicine research · 2026Article
- Ellagic acid can improve stroke by regulating gut microbiota.Metabolic brain disease · 2026Review
- Article
- Neuroprotective Mechanisms and Clinical Evidence for Acupuncture in Parkinson's Disease: A Systematic Review.Parkinson's disease · 2025Review
- Interstitial fluid transport in linea alba is involved in acupuncture-induced attenuation of ovarian hypofunction in aged rats.Frontiers in endocrinology · 2025Article
- Efficacy of acupuncture for motor dysfunction in early Parkinson's disease: protocol for a randomized, single-blind, sham-controlled clinical trial.Frontiers in medicine · 2025Article
- Corticostriatal glutamate-mediated dynamic therapeutic efficacy of electroacupuncture in a parkinsonian rat model.Clinical and translational medicine · 2024Article
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Abstract
backgroundMotor impairments are the defining cardinal features of Parkinson's disease (PD), resulting from malfunction of the cortico-basal ganglia circuit. Clinical data have demonstrated that electroacupuncture (EA) stimulation may benefit motor symptoms in PD without adverse effects. However, the specific effects of EA on PD and the underlying mechanisms remain largely unclear.
methodsThis study investigated the effects of EA stimulation during and after 100 Hz application in a rat model of PD created by unilateral injection of 6-hydroxydopamine (6-OHDA). To establish optimal treatment parameters of EA, motor behaviours were dynamically assessed using open field and rotarod tests. Additionally, we evaluated corticostriatal spine plasticity using immunoelectron microscopy and measured the levels of dopaminergic and glutamatergic neurotransmitters through microdialysis, in vivo electrochemistry and high-performance liquid chromatography. Neural activity dynamics were recorded by measuring local field potentials in both the motor cortex and the striatum. Furthermore, chemogenetic techniques were employed to manipulate corticostriatal glutamatergic neurons and clarify the mechanisms that contribute to the therapeutic benefits of EA in the PD rat model.
resultsChronic EA stimulation resulted in a gradual and long-lasting alleviation of motor symptoms, independent of nigrostriatal dopamine (DA) restoration. Notably, EA stimulation modulated corticostriatal spine plasticity and reduced excessive glutamate transmission in PD model rats. Moreover, EA effectively inhibited aberrant corticostriatal synchronised high-beta (25-40 Hz) oscillations, which serves as a pathological biomarker of PD. Conversely, chronic chemogenetic activation of corticostriatal glutamatergic neurons hindered these positive outcomes of EA treatment in PD model rats.
conclusionsThis study sheds light on the temporal dynamics and optimal parameters of EA treatment in PD. It emphasises the significance of inhibiting corticostriatal glutamate transmission in EA's therapeutic benefits for PD. Targeting glutamatergic neurons with EA holds promise as a non-dopaminergic intervention for managing motor symptoms and abnormal neural activity with PD. KEY POINTS: EA commonly protects dopaminergic neuronsby reducing neuroinflammation, oxidative stress, and apoptosis. New findings reveal that EA alleviates motor symptoms in a parkinsonian rat model without restoring striatal dopamine levels. EA effectively suppresses excessiveglutamate transmission and high-beta synchronization, contributing to motorsymptom relief. Activation of corticostriatalglutamatergic projections may hinder the efficacy of EA.
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