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. 2021 May 15;11(5):645. doi: 10.3390/brainsci11050645

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Possible mechanisms of action of transcranial ultrasound stimulation on the blink reflex circuit. Schematic representation of nuclei and circuits controlling blink reflex excitability (adapted from [21]) and possible mechanisms to explain the finding of reduced blink reflex inhibition after transcranial ultrasound stimulation (TUS). When delivered on the superior colliculus (SC), TUS may directly inhibit fibers originating from the SC and projecting to the nucleus raphe magnus (NRM) (1). Another possibility is that TUS exerts an excitatory effect at the level of GABAergic inhibitory synapses between substantia nigra (SN) projections and SC neurons (2). A third possible mechanism implies the facilitation of the activity of inhibitory interneurons located within the SC, thus reducing the output of the nucleus itself (3).