The after-effect of human theta burst stimulation is NMDA receptor dependent
Abstract
Objective To provide pharmacological evidence that the after-effects of theta burst stimulation (TBS) involve plasticity like changes in cortical synaptic connections, using the N-methyl-D-aspartate receptor antagonist memantine. Methods We performed a double blind, placebo-controlled study to evaluate the effect of memantine on the response of six healthy volunteers to TBS. We measured rest (RMT) and active (AMT) motor thresholds, and the amplitude of MEPs before and after continuous and intermittent TBS (cTBS/iTBS) after the administration of placebo or memantine. Results Memantine had no effect on RMT and AMT, while it blocked the suppressive effect of cTBS and the facilitatory effect of iTBS. Conclusions The effects of iTBS and cTBS rely on NMDARs to produce after-effects in the motor cortex of conscious humans. Significance The NMDA dependency of the after-effects of TBS adds to the understanding of the underlying mechanism of TBS, and suggests that these after-effects are likely to involve plasticity like changes at synaptic connections in motor cortex.
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MEP suppression following cTBS could be related to LTD-like processes mediated by NMDA receptors, as NMDA-r antagonist memantine was shown to block the after effects of cTBS.
“it has been suggested that MEP suppression following stimulation could be related to long-term depression (LTD)-like processes mediated by N-methyl-D-aspartate receptors (NMDA-r), as NMDA-r antogatonist memantine was shown to block the after effects of cTBS (Huang et al., 2007).”
From Theta burst stimulation to characterize changes in brain plasticity following mild traumatic brain injury: A proof-of-principle study (2015) · cites this paper as Huang et al., 2007
Modulation of GABA receptors and glutamate receptors has been proposed as a possible mechanism explaining excitability changes following TBS.
“Modulation of GABA receptors (Thickbroom, 2007) and glutamate receptors (Glu-r) (Huang et al., 2007) has also been proposed as a possible mechanism explaining excitability changes following TBS.”
From Theta burst stimulation to characterize changes in brain plasticity following mild traumatic brain injury: A proof-of-principle study (2015) · cites this paper as Huang et al., 2007
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- Authors
- Huang, Y.-Z., Chen, R.-S., Rothwell, J. C., & Wen, H.-Y.
- Affiliations
- Chang Gung University (TW)
- National Hospital for Neurology and Neurosurgery (GB)
- Corresponding author
- Huang, Ying-Zu
- Venue
- Clinical Neurophysiology
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 118
- Issue
- 5
- Pages
- 1028-1032
- ISSN
- 1388-2457 (ISSN-L)
- OpenAlex
- W2095128332
- Cited by
- 618
- References
- 1
- Citations by year
- 2026: 34 · 2025: 38 · 2024: 39 · 2023: 37 · 2022: 41 · 2021: 55 · 2020: 33 · 2019: 29 · 2018: 23 · 2017: 24 · 2016: 31 · 2015: 36 · 2014: 34 · 2013: 28 · 2012: 33
- FWCI
- 15.45
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Neurophysiology (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Science Council
- Topics
- Life Sciences › Neuroscience › Neurology › Transcranial Magnetic Stimulation Studies
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Keywords
- theta burst stimulation, NMDA receptor, memantine, motor cortex plasticity, motor evoked potentials, motor threshold, synaptic plasticity, continuous theta burst stimulation, intermittent theta burst stimulation
- MeSH terms
- Cerebral Cortex, Double-Blind Method, Electroencephalography, Humans, Memantine, Neuronal Plasticity, Rest, Synapses, Theta Rhythm, Receptors, N-Methyl-D-Aspartate, Excitatory Amino Acid Antagonists
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