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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Neurol. | doi: 10.3389/fneur.2019.00587

Modulation of resting connectivity between the mesial frontal cortex and basal ganglia

 Traian Popa1,  Laurel S. Morris2,  Rachel Hunt1, 3,  Zhi-De Deng4, 5,  Silvina Horovitz1,  Karin Mente1, Hitoshi Shitara1, Kwangyeol Baek2, Mark Hallett6 and Valerie Voon2*
  • 1Human Motor Control Section (HMCS) / National Institute of Neurological Diseases and Stroke (NINDS), National Institutes of Health (NIH), United States
  • 2Behavioural and Clinical Neuroscience Institute, Department of Psychology, Faculty of Biology, University of Cambridge, United Kingdom
  • 3Oakland University William Beaumont School of Medicine, United States
  • 4Non-Invasive Neuromodulation Unit, Experimental Therapeutics & Pathophysiology Branch, National Institute of Mental Health (NIMH), United States
  • 5Department of Psychiatry and Behavioral Sciences, School of Medicine, Duke University, United States
  • 6National Institute of Neurological Disorders and Stroke (NINDS), United States

Background: The mesial prefrontal cortex, cingulate cortex and the ventral striatum are key nodes of the human mesial fronto-striatal circuit involved in decision-making and executive function and pathological disorders. Here we ask whether deep wide-field repetitive transcranial magnetic stimulation (rTMS) targeting the mesial prefrontal cortex (MPFC) influences resting state functional connectivity.
Methods: In Study 1, we examined functional connectivity using resting state multi-echo and independent components analysis in 154 healthy subjects to characterize default connectivity in the MPFC and mid-cingulate cortex (MCC). In Study 2, we used inhibitory, 1Hz deep rTMS with the H7-coil targeting MPFC and dorsal anterior cingulate (dACC) in a separate group of 20 healthy volunteers and examined pre- and post-TMS functional connectivity using seed-based and independent components analysis.
Results: In Study 1, we show that MPFC and MCC have distinct patterns of functional connectivity with MPFC–ventral striatum showing negative, whereas MCC–ventral striatum showing positive functional connectivity. Low-frequency rTMS decreased functional connectivity of MPFC and dACC with the ventral striatum. We further showed enhanced connectivity between MCC and ventral striatum.
Conclusions: These findings emphasize how deep inhibitory rTMS using the H7-coil can influence underlying network functional connectivity by decreasing connectivity of the targeted MPFC regions, thus potentially enhancing response inhibition and decreasing drug-cue reactivity processes relevant to addictions. The unexpected finding of enhanced default connectivity between MCC and ventral striatum may be related to the decreased influence and connectivity between the MPFC and MCC. These findings are highly relevant to the treatment of disorders relying on the mesio-prefrontal-cingulo-striatal circuit.

Keywords: Cingulate cortex, Ventral striatum (VS), Mesial prefrontal cortex, Transcranial magnetic stimulation (rTMS), resting state connectivity MRI

Received: 18 Feb 2019; Accepted: 17 May 2019.

Edited by:

Matteo Bologna, Sapienza University of Rome, Italy

Reviewed by:

Alessandro Tessitore, Università degli Studi della Campania Luigi Vanvitelli Caserta, Italy
Ying-Zu Huang, Chang Gung University, Taiwan  

Copyright: © 2019 Popa, Morris, Hunt, Deng, Horovitz, Mente, Shitara, Baek, Hallett and Voon. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Valerie Voon, Behavioural and Clinical Neuroscience Institute, Department of Psychology, Faculty of Biology, University of Cambridge, Cambridge, CB2 3EB, United Kingdom, vv247@cam.ac.uk