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Neural circuit repair by low-intensity magnetic stimulation requires cellular magnetoreceptors and specific stimulation patterns.

ABSTRACT: Although electromagnetic brain stimulation is a promising treatment in neurology and psychiatry, clinical outcomes are variable, and underlying mechanisms are ill-defined, which impedes the development of new effective stimulation protocols. Here, we show, in vivo and ex vivo, that repetitive transcranial magnetic stimulation at low-intensity (LI-rTMS) induces axon outgrowth and synaptogenesis to repair a neural circuit. This repair depends on stimulation pattern, with complex biomimetic patterns being particularly effective, and the presence of cryptochrome, a putative magnetoreceptor. Only repair-promoting LI-rTMS patterns up-regulated genes involved in neuronal repair; almost 40% of were cryptochrome targets. Our data open a new framework to understand the mechanisms underlying structural neuroplasticity induced by electromagnetic stimulation. Rather than neuronal activation by induced electric currents, we propose that weak magnetic fields act through cryptochrome to activate cellular signaling cascades. This information opens new routes to optimize electromagnetic stimulation and develop effective treatments for different neurological diseases.

SUBMITTER: Dufor T

PROVIDER: S-EPMC6821463 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Neural circuit repair by low-intensity magnetic stimulation requires cellular magnetoreceptors and specific stimulation patterns.

Dufor T T Grehl S S Tang A D AD Doulazmi M M Traoré M M Debray N N Dubacq C C Deng Z-D ZD Mariani J J Lohof A M AM Sherrard R M RM

Science advances 20191030 10

Although electromagnetic brain stimulation is a promising treatment in neurology and psychiatry, clinical outcomes are variable, and underlying mechanisms are ill-defined, which impedes the development of new effective stimulation protocols. Here, we show, in vivo and ex vivo, that repetitive transcranial magnetic stimulation at low-intensity (LI-rTMS) induces axon outgrowth and synaptogenesis to repair a neural circuit. This repair depends on stimulation pattern, with complex biomimetic pattern ...[more]

PMID: 31692960

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Project description:Corticospinal output pathways have typically been considered to be the primary driver for voluntary movements of the hand/forearm; however, more recently, reticulospinal drive has also been implicated in the production of these movements. Although both pathways may play a role, the reticulospinal tract is thought to have stronger connections to flexor muscles than to extensors. Similarly, movements involuntarily triggered via a startling acoustic stimulus (SAS) are believed to receive greater reticular input than voluntary movements. To investigate a differential role of reticulospinal drive depending on movement type or acoustic stimulus, corticospinal drive was transiently interrupted using high-intensity transcranial magnetic stimulation (TMS) applied during the reaction time (RT) interval. This TMS-induced suppression of cortical drive leads to RT delays that can be used to assess cortical contributions to movement. Participants completed targeted flexion and extension movements of the wrist in a simple RT paradigm in response to a control auditory go signal or SAS. Occasionally, suprathreshold TMS was applied over the motor cortical representation for the prime mover. Results revealed that TMS significantly increased RT in all conditions. There was a significantly longer TMS-induced RT delay seen in extension movements than in flexion movements and a greater RT delay in movements initiated in response to control stimuli compared with SAS. These results suggest that the contribution of reticulospinal drive is larger for wrist flexion than for extension. Similarly, movements triggered involuntarily by an SAS appear to involve greater reticulospinal drive, and relatively less corticospinal drive, than those that are voluntarily initiated. NEW & NOTEWORTHY Through the use of the transcranial magnetic stimulation-induced silent period, we provide novel evidence for a greater contribution of reticulospinal drive, and a relative decrease in corticospinal drive, to movements involuntarily triggered by a startle compared with voluntary movements. These results also provide support for the notion that both cortical and reticular structures are involved in the neural pathway underlying startle-triggered movements. Furthermore, our results indicate greater reticulospinal contribution to wrist flexion than extension movements.

Dataset Information

Neural circuit repair by low-intensity magnetic stimulation requires cellular magnetoreceptors and specific stimulation patterns.

Publications

Neural circuit repair by low-intensity magnetic stimulation requires cellular magnetoreceptors and specific stimulation patterns.

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