Cortical Mechanisms of Single-Pulse Transcranial Magnetic Stimulation in Migraine
Autor: | Kim I. Chisholm, Martyn G Jones, Joseph O Lloyd, Giorgio Lambru, Adnan Al-Kaisy, Beatrice Oehle, Bright N Okine, Anna P. Andreou, Stephen B. McMahon |
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Rok vydání: | 2020 |
Předmět: |
Male
0301 basic medicine Migraine Disorders medicine.medical_treatment Glutamic Acid glutamate Rats Sprague-Dawley Mice GABA 03 medical and health sciences 0302 clinical medicine medicine Animals Premovement neuronal activity Pharmacology (medical) Migraine treatment Migraine Pharmacology GABAA receptor Chemistry Cortical Spreading Depression Iontophoresis medicine.disease Transcranial Magnetic Stimulation Rats Cortex (botany) Mice Inbred C57BL Transcranial magnetic stimulation cortex 030104 developmental biology Visual cortex medicine.anatomical_structure Cortical spreading depression Female Original Article Occipital Lobe Neurology (clinical) Neuroscience 030217 neurology & neurosurgery |
Zdroj: | Neurotherapeutics |
ISSN: | 1878-7479 1933-7213 |
Popis: | Single-pulse transcranial magnetic stimulation (sTMS) of the occipital cortex is an effective migraine treatment. However, its mechanism of action and cortical effects of sTMS in migraine are yet to be elucidated. Using calcium imaging and GCaMP-expressing mice, sTMS did not depolarise neurons and had no effect on vascular tone. Pre-treatment with sTMS, however, significantly affected some characteristics of the cortical spreading depression (CSD) wave, the correlate of migraine aura. sTMS inhibited spontaneous neuronal firing in the visual cortex in a dose-dependent manner and attenuated l-glutamate-evoked firing, but not in the presence of GABAA/B antagonists. In the CSD model, sTMS increased the CSD electrical threshold, but not in the presence of GABAA/B antagonists. We first report here that sTMS at intensities similar to those used in the treatment of migraine, unlike traditional sTMS applied in other neurological fields, does not excite cortical neurons but it reduces spontaneous cortical neuronal activity and suppresses the migraine aura biological substrate, potentially by interacting with GABAergic circuits. Electronic supplementary material The online version of this article (10.1007/s13311-020-00879-6) contains supplementary material, which is available to authorized users. |
Databáze: | OpenAIRE |
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