Neural Circuit Repair by Low-Intensity rTMS

2022 ◽  
Author(s):  
A. M. Lohof ◽  
T. Dufor ◽  
R. M. Sherrard
Keyword(s):  
Neural Circuit ◽  
Low Intensity

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

2019 ◽  
Vol 5 (10) ◽  
pp. eaav9847 ◽  
Author(s):  
T. Dufor ◽  
S. Grehl ◽  
A. D. Tang ◽  
M. Doulazmi ◽  
M. Traoré ◽  
...  
Keyword(s):  
Magnetic Stimulation ◽  
Neural Circuit ◽  
Ex Vivo ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Neurological Diseases ◽  
Low Intensity ◽  
Electromagnetic Stimulation ◽  
Weak Magnetic Fields ◽  
Underlying Mechanisms

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.

scholarly journals Neural circuit repair by low-intensity magnetic stimulation requires cryptochrome

2018 ◽  
Author(s):  
Tom Dufor ◽  
Stephanie Grehl ◽  
Alexander D Tang ◽  
Mohamed Doulazmi ◽  
Massiré Traoré ◽  
...  
Keyword(s):  
Electric Fields ◽  
Magnetic Stimulation ◽  
Target Genes ◽  
Neural Circuit ◽  
Ex Vivo ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Altered Expression ◽  
Low Intensity ◽  
Promising Treatment

AbstractMagnetic brain stimulation is a promising treatment in neurology and psychiatry, but clinical outcomes are variable. Unfortunately, mechanisms underlying magnetic stimulation effects are ill-defined, which impedes the development of stimulation protocols appropriate for different neurological conditions. 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 patterns being particularly effective, and its mechanism requires the presence of cryptochrome (Cry), a putative magneto-receptor. Effective LI-rTMS patterns altered expression of Cry target genes known to promote neuronal repair. Because LI-rTMS generates electric fields too weak to depolarise neurons, these findings indicate that the magnetic field itself induces the repair. Our data open a new framework for magnetic stimulation - cryptochrome-mediated molecular and structural neuroplasticity. This information suggests new routes to treatments specific for each neurological disease.

Low-Intensity Cognitive Behavioral Therapy

2017 ◽  
Vol 2 (1) ◽  
pp. 31-36
Author(s):  
Pascal Wabnitz ◽  
Michael Schulz ◽  
Michael Löhr ◽  
André Nienaber
Keyword(s):  
Cognitive Behavioral Therapy ◽  
Behavioral Therapy ◽  
Cognitive Behavioral ◽  
Low Intensity

Maori adaptation of a low intensity mental health intervention in primary care

2012 ◽  
Author(s):  
Fiona Mathieson ◽  
Kara Mihaere ◽  
Sunny Collings ◽  
Anthony Dowell ◽  
James Stanley
Keyword(s):  
Mental Health ◽  
Primary Care ◽  
Health Intervention ◽  
Mental Health Intervention ◽  
Low Intensity

Inhibition rather than Enhancement of Hemostatic System Activation during Initiation of Oral Anticoagulant Treatment

1997 ◽  
Vol 77 (04) ◽  
pp. 685-689 ◽  
Author(s):  
Paul A Kyrle ◽  
Johannes Brockmeier ◽  
Ansgar Weltermann ◽  
Sabine Eichinger ◽  
Wolfgang Speiser ◽  
...  
Keyword(s):  
High Intensity ◽  
Oral Anticoagulant ◽  
Protein C ◽  
Venous Blood ◽  
Rapid Decline ◽  
Oral Anticoagulant Treatment ◽  
Shed Blood ◽  
Low Intensity ◽  
Hemostatic System ◽  
System Activation

SummaryCoumarin-induced skin necrosis is believed to be due to a transient hypercoagulable state resulting from a more rapid decline of the protein C activity relative to that of coagulation factors (F) II, IX and X during initiation of oral anticoagulant therapy. We studied hemostatic system activation during early oral anticoagulant treatment with a technique that investigates coagulation activation in the microcirculation.We determined in 10 healthy volunteers the concentrations of prothrombin fragment F1+2 (f1.2) and thrombin-antithrombin complex (TAT) in blood emerging from an injury of the microvasculature (bleeding time incision) before and after initiation of both high-inten- sity and low-intensity coumarin therapy. In addition, f1.2, TAT, activated F VII (F Vila) and the activities of FII, F VII, F X and protein C were measured in venous blood.A rapid decline of F VII and protein C was observed in venous blood with activities at 24 h of 7 ± 1% and 43 ± 2%, respectively, during the high-intensity regimen. A 20 to 30% reduction of f1.2 and TAT was seen in venous blood at 72 h with no major difference between the high- and the low-intensity regimen. F Vila levels were substantially affected by anticoagulation with a >90% reduction at 48 h during the high-intensity regimen. Following high-intensity coumarin, a >50% decrease in the fl.2 and TAT levels was found in shed blood at 48 h suggesting substantial inhibition of thrombin generation during early oral anticoagulation. An increase in the f1.2 and TAT levels was seen neither in shed blood nor in venous blood.Our data do not support the concept of a transient imbalance between generation and inhibition of thrombin as the underlying pathomechanism of coumarin-induced skin nekrosis.

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