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Updated: May 20, 2026

Standardized Induction and Assessment of Long-term Potentiation-like Cortical Plasticity Using Transcranial Magnetic Stimulation
Published on: November 7, 2025
Effects of lamotrigine on human motor cortex plasticity
Igor Delvendahl1, Hannes Lindemann, Tonio Heidegger
1European Neuroscience Institute Göttingen, Göttingen, Germany.
Lamotrigine (LTG) affects brain plasticity differently in individuals. This mood stabilizer reduces long-term potentiation (LTP)-like responses and alters long-term depression (LTD)-like responses, impacting neuronal plasticity.
Area of Science:
- Neuroscience
- Psychopharmacology
Background:
- Lamotrigine (LTG) is an anticonvulsant also used as a mood stabilizer.
- Mood disorders may involve impaired neuronal plasticity, including long-term potentiation (LTP) and long-term depression (LTD).
- The precise effects of LTG on human neuronal plasticity are not fully understood.
Purpose of the Study:
- To investigate the impact of a single oral dose of LTG (300 mg) on motor cortical plasticity in healthy adults.
- To determine if LTG modulates plasticity differently based on an individual's baseline response to plasticity-inducing stimulation.
Main Methods:
- A placebo-controlled, randomized, double-blind crossover study involving 26 healthy adults.
- Paired associative stimulation (PAS(25)) was used to induce LTP-like plasticity.
- Motor evoked potential (MEP) amplitudes were measured before and after PAS(25) to assess plasticity.
Main Results:
- LTG significantly reduced the LTP-like increase in MEP amplitudes in individuals prone to LTP.
- LTG also reduced the LTD-like decrease in MEP amplitudes in individuals prone to LTD, with some showing an MEP increase.
- These findings indicate LTG differentially modulates cortical plasticity based on individual response.
Conclusions:
- LTG differentially modulates non-invasively stimulated cortical plasticity in humans.
- The drug's effects depend on an individual's intrinsic capacity for LTP-like or LTD-like plasticity.
- This modulation may underlie LTG's efficacy in epilepsy and mood disorders by downregulating excessive LTP or LTD.
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