The effect of repetitive transcranial magnetic stimulation on long-term potentiation in rat hippocampus depends on stimulus intensity

2003 ◽  
Vol 993 (1-2) ◽  
pp. 222-226 ◽  
Author(s):  
Mari Ogiue-Ikeda ◽  
Suguru Kawato ◽  
Shoogo Ueno
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Stimulus Intensity ◽  
Magnetic Stimulation ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Term Potentiation

scholarly journals Physiological correlates of neuro- and magnetic stimulation in therapy of epilepsy

2020 ◽  
Vol 28 (1) ◽  
pp. 88-98
Author(s):  
Nataliya D. Sorokina ◽  
Sergey S. Pertsov ◽  
Gennadiy V. Selitskiy
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Experimental Studies ◽  
Low Frequency ◽  
Long Term Potentiation ◽  
Physiological Mechanisms ◽  
Term Potentiation ◽  
Magnetic Action

In the literature survey, non-pharmaceutical methods of therapy of epilepsy are considered including electrostimulation of vagus nerve, exposure to magnetic field and transcranial magnetic stimulation (TMS). Correlates of the effectiveness of electro- and magnetic stimulation are electrophysiological parameters, clinical data and influence on the mental and cognitive functions. Use of repetitive transcranial magnetic stimulation in addition to antiepileptic drugs has a certain ground. According to modern understanding and the results of experimental studies, the mechanism of modulator inhibitory alterations is associated with a potential of TMS to cause long-term synaptic depression or long-term potentiation. These long-lasting phenomena probably underlie anticonvulsant effects of low frequency magnetic stimulation. Inclusion of physiologists and neurophysiologists into the research will permit to solve such an important problem as a study of physiological mechanisms of the effectiveness of non-pharmacological electro- and magnetic action in epilepsy.

Mechanisms of human motor cortex facilitation induced by subthreshold 5-Hz repetitive transcranial magnetic stimulation

2013 ◽  
Vol 109 (12) ◽  
pp. 3060-3066 ◽  
Author(s):  
Martin Sommer ◽  
Milena Rummel ◽  
Christoph Norden ◽  
Holger Rothkegel ◽  
Nicolas Lang ◽  
...  
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Motor Cortex ◽  
Magnetic Stimulation ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Long Term Potentiation ◽  
Human Motor Cortex ◽  
Term Potentiation ◽  
Human Motor ◽  
Extensor Carpi Radialis

Our knowledge about the mechanisms of human motor cortex facilitation induced by repetitive transcranial magnetic stimulation (rTMS) is still incomplete. Here we used pharmacological conditioning with carbamazepine, dextrometorphan, lorazepam, and placebo to elucidate the type of plasticity underlying this facilitation, and to probe if mechanisms reminiscent of long-term potentiation are involved. Over the primary motor cortex of 10 healthy subjects, we applied biphasic rTMS pulses of effective posterior current direction in the brain. We used six blocks of 200 pulses at 5-Hz frequency and 90% active motor threshold intensity and controlled for corticospinal excitability changes using motor-evoked potential (MEP) amplitudes and latencies elicited by suprathreshold pulses before, in between, and after rTMS. Target muscle was the dominant abductor digiti minimi muscle; we coregistered the dominant extensor carpi radialis muscle. We found a lasting facilitation induced by this type of rTMS. The GABAergic medication lorazepam and to a lesser extent the ion channel blocker carbamazepine reduced the MEP facilitation after biphasic effective posteriorly oriented rTMS, whereas the N-methyl-d-aspartate receptor-antagonist dextrometorphan had no effect. Our main conclusion is that the mechanism of the facilitation induced by biphasic effective posterior rTMS is more likely posttetanic potentiation than long-term potentiation. Additional findings were prolonged MEP latency under carbamazepine, consistent with sodium channel blockade, and larger MEP amplitudes from extensor carpi radialis under lorazepam, suggesting GABAergic involvement in the center-surround balance of excitability.

Effect of caffeine on long-term potentiation-like effects induced by quadripulse transcranial magnetic stimulation

2018 ◽  
Vol 237 (3) ◽  
pp. 647-651 ◽  
Author(s):  
Ritsuko Hanajima ◽  
Nobuyuki Tanaka ◽  
Ryosuke Tsutsumi ◽  
Yuichiro Shirota ◽  
Takahiro Shimizu ◽  
...  
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Biophysical modeling of neural plasticity induced by transcranial magnetic stimulation

2017 ◽  
Author(s):  
Marcus T. Wilson ◽  
Ben D. Fulcher ◽  
Park K. Fung ◽  
Peter A. Robinson ◽  
Alex Fornito ◽  
...  
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Numerical Models ◽  
Long Term Potentiation ◽  
Stimulus Interval ◽  
Paired Associative Stimulation ◽  
Dependent Plasticity ◽  
Term Potentiation ◽  
Theta Burst

AbstractTranscranial magnetic stimulation (TMS) is a widely used noninvasive brain stimulation method capable of inducing plastic reorganisation of cortical circuits in humans. Changes in neural activity following TMS are often attributed to synaptic plasticity (e.g long-term potentiation and depression; LTP/LTD). However, the precise way in which synaptic processes such as LTP/LTD modulate the activity of large populations of neurons, as stimulated en masse by TMS, are unclear. The recent development of biophysically-informed models, which capture the physiological properties of TMS-induced plasticity using mathematics, provide an excellent framework for reconciling synaptic and macroscopic plasticity. In this article, we overview the TMS paradigms used to induce plasticity, and their limitations. We then describe the development of biophysically-based numerical models of the mechanisms underlying LTP/LTD on population-level neuronal activity, and the application of these models to TMS plasticity paradigms, including theta burst and paired associative stimulation. Finally, we outline how modeling can complement experiment to improve mechanistic understandings and optimize outcomes of TMS-induced plasticity.AbbreviationsTMStranscranial magnetic stimulationLTPlong-term potentiationLTDlong-term depressionrTMSrepetitive TMSTBStheta burst stimulationPASpaired-associative stimulationMEPmotor-evoked potentialcTBScontinuous TBSiTBSintermittent TBSNMDAn-methyl-d-aspartateCaDPcalcium dependent plasticityEEGelectroencephalographyMRImagnetic resonance imagingSTDPspike timing dependent plasticityBCMBienenstock-Cooper-MunroGABAgamma-aminobutyric-acidISIinter-stimulus interval

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