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Updated: Jun 29, 2026

Repetitive Transcranial Magnetic Stimulation to the Unilateral Hemisphere of Rat Brain
Published on: October 22, 2016
From Imbalance to Intervention: Neurochemical Alterations in Canine Anxiety and Its Modulation by Repetitive
Sofie Salden1, Yangfeng Xu1, Ann Van Eeckhaut2
1Department of Morphology, Imaging, Orthopedics, Rehabilitation, and Nutrition, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium; Department of Head and Skin, Ghent Experimental Psychiatry (GHEP) Lab, Ghent University, Ghent, Belgium.
Objectives:
Accelerated high-frequency repetitive transcranial magnetic stimulation (aHF-rTMS) is an emerging modality in both human and veterinary medicine. Although previous studies show brain changes and behavioral improvements in healthy and patient dogs, the effects of aHF-rTMS on neurotransmitter levels remain poorly understood. This study aimed to compare monoaminergic metabolite profiles in healthy and anxious dogs, and to evaluate short-term, long-term, and dose-dependent effects of aHF-rTMS on these metabolites.
Materials And Methods:
A total of 79 dogs were included, comprising 59 healthy controls and 20 anxious dogs. Cerebrospinal fluid samples were collected to measure dopaminergic (3,4-dihydroxyphenylacetic acid [DOPAC] and homovanillic acid [HVA]) and serotonergic (5-hydroxyindoleacetic acid [5-HIAA]) metabolites before and after various aHF-rTMS protocols with varying dosing and duration. Generalized linear mixed-effects models were used to assess baseline differences and stimulation-induced changes across protocols and timepoints.
Results:
Patient dogs consistently showed lower baseline levels of all three metabolites (DOPAC, HVA, and 5-HIAA) than healthy controls, supporting a neurochemical basis for canine anxiety. Furthermore, neuromodulatory effects of aHF-rTMS were selective and dependent on protocol and timing. In healthy dogs, the short-term stimulation increased 5-HIAA whereas longer protocols reduced HVA. In patient dogs, long-term follow-up revealed significant fluctuations in DOPAC, whereas HVA and 5-HIAA remained stable.
Conclusions:
These findings indicate baseline monoaminergic deficits in anxious dogs and support a neurochemical basis for canine anxiety. Moreover, aHF-rTMS induces distinct, state- and duration-dependent neurochemical responses. Overall, this study provides novel insights into the neurobiology of anxious dogs and supports further investigation of aHF-rTMS as a neuromodulatory approach in dogs with translational relevance.
