scholarly journals Transcranial magnetic stimulation promotes the proliferation of dopaminergic neuronal cells in vitro

AIP Advances ◽  
2018 ◽  
Vol 8 (5) ◽  
pp. 056709 ◽  
Author(s):  
Xiaojing Zhong ◽  
Jie Luo ◽  
Priyam Rastogi ◽  
Anumantha G. Kanthasamy ◽  
David C. Jiles ◽  
...  
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Neuronal Cells

EXTH-47. SAFETY AND EFFECTS OF TRANSCRANIAL MAGNETIC STIMULATION ON GLIOBLASTOMA MEASURED IN VITRO

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi173-vi174
Author(s):  
Christen O'Neal ◽  
Sydney Scott ◽  
Tressie Stephens ◽  
Patrick McKernan ◽  
Arpan Chakraborty ◽  
...  
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Fields ◽  
Cell Lines ◽  
Magnetic Stimulation ◽  
Motor Deficits ◽  
Postoperative Rehabilitation ◽  
Low Frequencies ◽  
Electrical Currents ◽  
Stimulation Parameters

Abstract BACKGROUND Although gross total resection (GTR) with chemoradiation is the standard of care for treating glioblastoma (GBM), tumor infiltration and treatment sequelae can impair activity of eloquent regions. Transcranial magnetic stimulation (TMS) has been explored as an adjunct therapy to rehabilitation for post-stroke motor deficits. TMS could be effective for postoperative rehabilitation in GBM, but its effect on GBM cells has not been evaluated. While TMS utilizes magnetic fields to induce electrical currents at low frequencies to cause neuronal excitation or inhibition, tumor-treating fields (TTF) utilize electrical currents with intermediate frequency to exert anti-mitotic effects, demonstrating promise as an adjunctive therapy in recurrent GBM. Although similarities exist between electrical and magnetic fields, the effects of magnetically induced electrical currents at low frequencies via TMS must be studied systematically in vitro on GBM cell lines. METHODS We studied the effect of theta burst stimulation (TBS), a form of patterned TMS, on in vitro G55 cell viability using colony forming assays. We compared TMS-treated cells to controls using a combination of parameters: continuous versus intermittent TBS (cTBS and iTBS), 300 versus 600 pulses, stimulation intensity of 32% versus 60%, and no pre-TMS chemotherapy versus 100 nM or 100 µM temozolomide (TMZ). Viability measurements between controls and TMS were analyzed using analysis of variance (ANOVA). Independent t-tests were used to analyze effects of stimulation parameters on viability percent difference within each TMZ condition. RESULTS There was no statistically significant increase in viability between control and TMS conditions for any of the stimulation parameters (+/- TMZ) while some showed decreased viability of GBM cells. CONCLUSIONS TMS did not significantly increase GBM viability compared to controls. Future studies include validation in other cell lines and characterization of the effects of stimulation parameters in conjunction with TMZ and dexamethasone, (often administered concurrently with GBM treatment).

scholarly journals Design and demonstration in vitro of mouse-specific Transcranial Magnetic Stimulation coil

2020 ◽  
Author(s):  
Farah A. Khokhar ◽  
Logan J. Voss ◽  
D. Alistair Steyn-Ross ◽  
Marcus T. Wilson
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Copper Wire ◽  
Animal Experiments ◽  
Brain Slices ◽  
Iron Core ◽  
Hall Probe ◽  
Measured Temperature ◽  
Frequency Changes

AbstractBackgroundTranscranial Magnetic Stimulation (TMS) is a technique used to treat different neurological disorders non-invasively. A pulsed current to a coil induces an E-field. Underlying biophysical effects of TMS are unclear. Therefore, animal experiments are needed; however, making small TMS coils suitable for mice is difficult because their field strengths are much lower than for human sized coils.Objectives/HypothesisWe aimed to design and demonstrate a mouse-specific coil that can generate high and focused E-field.MethodsWe designed a tapered TMS coil of 50 turns of 0.2 mm diameter copper wire around a 5 mm diameter tapered powdered iron core and discharged a 220 µF capacitor at 50 V through it. We measured B-field with a Hall probe and induced E-field with a wire loop. We measured temperature rise with a thermocouple. We applied 1200 pulses of cTBS and iTBS to mouse brain slices and analysed how spontaneous electrical activity changed.ResultsThe coil gave maximum B-field of 760 mT and maximum E-field of 32 V/m, 2 mm below the coil, at 50 V power supply with a temperature increase of 20 degrees after 1200 pulses of cTBS. cTBS reduced frequency of spontaneous activity up to 20 minutes after stimulation and iTBS increased frequency of up to 20 minutes after stimulation. No frequency changes occurred after 20 minutes. No frequency changes in amplitude of spontaneous events were found.ConclusionThe design generated focused fields strong enough to modulate brain activity in vitro.

scholarly journals Repetitive transcranial magnetic stimulation improves neurological function after cerebral ischemia in rats by increasing CREB-regulated TrkB via activation of cAMP/PKA and Ca2+/CaMKIV signaling pathways

2019 ◽  
Author(s):  
Lisha Chang ◽  
Zhaowang An ◽  
Jiang Zhang ◽  
Fuling Zhou ◽  
Dali Wang ◽  
...  
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Cerebral Ischemia ◽  
Magnetic Stimulation ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Glucose Deprivation ◽  
Artery Occlusion ◽  
Neurological Function ◽  
Nerve Recovery ◽  
Underlying Mechanisms

Abstract Background: Cerebral ischemia is the most prevalent form of clinical stroke. Repetitive transcranial magnetic stimulation (rTMS) can modulate excitability of the cerebral cortex, and this effect is maintained after the stimulation is terminated. However, the underlying mechanisms of rTMS in cerebral ischemia remain unclear. Methods: Herein, we identified the effect of rTMS on cerebral ischemia and further explored the underlying mechanisms. An in vitro model was established using primary cultured neurons under conditions of oxygen-glucose deprivation (OGD), followed by 1 Hz or 10 Hz rTMS treatment. The levels of CREB, PKA and CaMKIV were depleted in neurons to explore the underlying regulatory mechanisms of TrkB by rTMS via CREB. A rat model of cerebral ischemia was established by middle cerebral artery occlusion (MCAO) and the rats were treated with 1 Hz or 10 Hz rTMS to investigate the effect of rTMS on neurobehavior, CREB expression, and cAMP/PKA and Ca 2+ /CaMKIV pathways. Results: rTMS was observed to promote nerve recovery ability in rats with cerebral ischemia, which was accompanied by high expression of TrkB. In OGD-treated neurons, rTMS activated CREB by upregulating cAMP/PKA and Ca 2+ /CaMKIV pathways. Moreover, rTMS induced the activation of CREB to upregulate TrkB. In MCAO rats, rTMS increased the CREB expression, enhanced cAMP, PKA and CaMKIV phosphorylation, and promoted the binding of CREB to TrkB. Conclusions: Taken together, rTMS upregulated CREB and TrkB to improve neurological function in rats with cerebral ischemia by activating cAMP/PKA and Ca 2+ /CaMKIV pathways, which could be of great significance for cerebral ischemia therapy.

scholarly journals Transcranial Magnetic stimulation (TMS) modulates functional activity of SH-SY5Y cells: An in vitro model provides support for assumed excitability changes

2020 ◽  
Author(s):  
Alix C. Thomson ◽  
Tom A. de Graaf ◽  
Teresa Schuhmann ◽  
Gunter Kenis ◽  
Alexander T. Sack ◽  
...  
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Calcium Imaging ◽  
Magnetic Stimulation ◽  
Neuron Model ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Patient Specific ◽  
Single Subject ◽  
Fluorescence Response ◽  
Human Neuron

AbstractRepetitive Transcranial Magnetic Stimulation (rTMS) is an established neuromodulation technique, using electromagnetic pulses that, depending on the precise parameters, are assumed to lead to lasting neural excitability changes. rTMS has widespread applications in both research and therapy, where it has been FDA approved and is considered a first-line treatment for depression, according to recent North American and European guidelines. However, these assumed excitability effects are often difficult to replicate, and highly unreliable on the single subject/patient level. Given the increasing application of rTMS, especially in clinical practice, the absence of a method to unequivocally determine effects of rTMS on human neuronal excitability is problematic. We have taken a first step in addressing this bottleneck, by administering excitatory and inhibitory rTMS protocols, iTBS and cTBS, to a human in vitro neuron model; differentiated SH-SY5Y cells. We use live calcium imaging to assess changes in neural activity following stimulation, through quantifying fluorescence response to chemical depolarization. We found that iTBS and cTBS have opposite effects on fluorescence response; with iTBS increasing and cTBS decreasing response to chemical depolarization. Our results are promising, as they provide a clear demonstration of rTMS after-effects in a living human neuron model. We here present an in-vitro live calcium imaging setup that can be further applied to more complex human neuron models, for developing and evaluating subject/patient-specific brain stimulation protocols.

Repetitive Transcranial Magnetic Stimulation of the Brain

2016 ◽  
Vol 23 (1) ◽  
pp. 82-94 ◽  
Author(s):  
Alexander Tang ◽  
Gary Thickbroom ◽  
Jennifer Rodger
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Therapeutic Potential ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Experimental Studies ◽  
Basic Research ◽  
In Vitro Models ◽  
In Vivo Studies

Since the development of transcranial magnetic stimulation (TMS) in the early 1980s, a range of repetitive TMS (rTMS) protocols are now available to modulate neuronal plasticity in clinical and non-clinical populations. However, despite the wide application of rTMS in humans, the mechanisms underlying rTMS-induced plasticity remain uncertain. Animal and in vitro models provide an adjunct method of investigating potential synaptic and non-synaptic mechanisms of rTMS-induced plasticity. This review summarizes in vitro experimental studies, in vivo studies with intact rodents, and preclinical models of selected neurological disorders—Parkinson’s disease, depression, and stroke. We suggest that these basic research findings can contribute to the understanding of how rTMS-induced plasticity can be modulated, including novel mechanisms such as neuroprotection and neurogenesis that have significant therapeutic potential.

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