The brain is not static. It continuously adapts to experience, learning and activity. Magnetic stimulation gives researchers a way to study and influence some of those adaptive processes.
Neuroplasticity describes the nervous system’s ability to change in response to activity and experience. It is fundamental to learning and adaptation, and it is also one of the central biological concepts used to understand the lasting after-effects of TMS.
Human motor-cortex studies show that repetitive TMS can produce changes in cortical excitability that continue after stimulation has ended. High-frequency rTMS is generally associated with increased cortical excitability and LTP-like effects, while stimulation around 1 Hz typically reduces excitability and is described as LTD-like. Huang et al. demonstrated a similar direction-dependent pattern with theta burst stimulation: intermittent TBS increased motor-evoked potentials, whereas continuous TBS reduced them. [1-3]
These effects are called LTP-like and LTD-like because they resemble physiological patterns associated with long-term potentiation and long-term depression. They are not direct measurements of synaptic LTP or LTD in the living human brain. [1-3]
From electrical activity to cellular adaptation
Long-lasting neural adaptation requires more than a momentary change in electrical activity. Fundamental neuroscience links activity-dependent plasticity to receptor signaling, intracellular calcium pathways, gene transcription, protein synthesis and structural changes at synapses. Experimental magnetic-stimulation studies provide additional mechanistic context. [3]
Thomson et al. applied TBS-patterned magnetic stimulation to a differentiated human neuron-like cell model and found protocol-specific changes in plasticity-related gene expression after iTBS. In the same study, neurite length and branching changed over time but did not show a significant overall effect of stimulation condition. Lenz et al. demonstrated plastic changes at inhibitory synapses after repetitive magnetic stimulation in experimental neuronal preparations, while Galanis et al. reported potentiation of excitatory synaptic transmission in mouse organotypic brain tissue cultures. [4-6]
BDNF, a neurotrophin closely involved in activity-dependent plasticity, has also been studied. Wang et al. reported enhanced BDNF-TrkB signaling after repeated 5-Hz rTMS in rat prefrontal cortex and lymphocytes; in healthy human participants, motor-cortex rTMS altered resting motor threshold and was associated with changes in BDNF-TrkB signaling measured in lymphocytes. The peripheral biomarker is not a direct measurement of BDNF signaling inside the human brain. [7]
Cheeran et al. further showed that the common BDNF Val66Met polymorphism influenced responses to several plasticity-inducing stimulation protocols in human motor cortex, illustrating that individual biology can contribute to variability in TMS after-effects. [8]
Taken together, the research supports a compelling idea: magnetic stimulation does more than briefly activate neurons. Repetitive stimulation can produce after-effects in neural excitability and engage biological processes associated with adaptation. This is why neuroplasticity is such a useful foundation for understanding the broader TMS literature. [1-8]
Stress regulation, mood, sleep, cognition and behavioral control are not isolated functions. They depend on interacting neural networks that adapt with experience. TMS does not simply “increase neuroplasticity,” and plasticity should not be treated as a direct wellness outcome. Rather, it provides a biological framework for understanding how repeated, targeted stimulation can lead to effects that continue beyond the stimulation itself and why different targets and protocols can produce different functional outcomes.
In that sense, neuroplasticity connects many of the wellness-relevant observations described across this series: recovery from stress, changes in mood-related measures, sleep quality, cognitive performance and behavioral control. The science is still evolving, but the common thread is the brain’s capacity to adapt.
References
[1] Huang YZ, Edwards MJ, Rounis E, Bhatia KP, Rothwell JC. Theta burst stimulation of the human motor cortex. Neuron. 2005; 45(2):201-206. doi:10.1016/j.neuron. 2004.12.033.
[2] Chen R, Classen J, Gerloff C, et al. Depression of motor cortex excitability by low-frequency transcranial magnetic stimulation. Neurology. 1997; 48(5):1398-1403. doi:10.1212/WNL.48.5.1398.
[3] Hoogendam JM, Ramakers GMJ, Di Lazzaro V. Physiology of repetitive transcranial magnetic stimulation of the human brain. Brain Stimul. 2010; 3(2):95-118. doi:10.1016/j.brs.2009.10.005.
[4] Thomson AC, Kenis G, Tielens S, et al. Transcranial Magnetic Stimulation-Induced Plasticity Mechanisms: TMS-Related Gene Expression and Morphology Changes in a Human Neuron-Like Cell Model. Front Mol Neurosci. 2020; 13:528396. doi:10.3389/fnmol.2020.528396.
[5] Lenz M, Galanis C, Muller-Dahlhaus F, et al. Repetitive magnetic stimulation induces plasticity of inhibitory synapses. Nat Commun. 2016; 7:10020. doi:10.1038/ncomms10020.
[6] Galanis C, Hananeia N, Lenz M, et al. Repetitive magnetic stimulation induces plasticity of excitatory synapses through cooperative pre- and postsynaptic activity. Brain Stimul. 2025; 18(5):1641-1650. doi:10.1016/j.brs.2025.08.019.
[7] Wang HY, Crupi D, Liu J, et al. Repetitive Transcranial Magnetic Stimulation Enhances BDNF-TrkB Signaling in Both Brain and Lymphocyte. J Neurosci. 2011; 31(30):11044-11054. doi:10.1523/JNEUROSCI.2125-11.2011.
[8] Cheeran B, Talelli P, Mori F, et al. A common polymorphism in the brain-derived neurotrophic factor gene (BDNF) modulates human cortical plasticity and the response to rTMS. J Physiol. 2008; 586(23):5717-5725. doi:10.1113/jphysiol.2008.159905.
