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Front Physiol. 2017 Jun 30;8:457. doi: 10.3389/fphys.2017.00457. eCollection 2017.

Mechanism of Action for rTMS: A Working Hypothesis Based on Animal Studies.

Author information

1
Department of Experimental Neurology and Clinical Neurophysiology, Centro Neurolesi Bonino Pulejo (IRCCS)Messina, Italy.
2
Department of Physiology, Pharmacology and Neuroscience, Sophie Davis School for Biomedical Education at City College of New York, City University of New YorkNew York, NY, United States.
3
The Fresco Institute for Parkinson's and Movement Disorders, NYU Langone Medical CenterNew York, NY, United States.
4
Department of Neurology, Nuovo Garibaldi HospitalCatania, Italy.
5
Department of Biomedical, Dental Sciences and Morphological and Functional Images, University of MessinaMessina, Italy.

Abstract

Experiments in rodents have elucidated some of the molecular mechanisms underlying repetitive transcranial magnetic stimulation (rTMS). These studies may be useful in a translational perspective so that future TMS studies in rodents can closely match human TMS protocols designed for therapeutic purposes. In the present work we will review the effects of rTMS on glutamate neurotransmission which in turn induce persistent changes in synaptic activity. In particular, we will focus on the role of NMDA and non-NMDA transmission and on the permissive role of BDNF-TrKB interaction in the rTMS induced after-effects.

KEYWORDS:

BDNF-TrKB signaling; NMDA; TMS; long-term potentiation; neuroprotection

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