Abstract
Transcranial 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.
- TMS
- transcranial magnetic stimulation
- LTP
- long-term potentiation
- LTD
- long-term depression
- rTMS
- repetitive TMS
- TBS
- theta burst stimulation
- PAS
- paired-associative stimulation
- MEP
- motor-evoked potential
- cTBS
- continuous TBS
- iTBS
- intermittent TBS
- NMDA
- n-methyl-d-aspartate
- CaDP
- calcium dependent plasticity
- EEG
- electroencephalography
- MRI
- magnetic resonance imaging
- STDP
- spike timing dependent plasticity
- BCM
- Bienenstock-Cooper-Munro
- GABA
- gamma-aminobutyric-acid
- ISI
- inter-stimulus interval