TMS-EEG signatures of glutamatergic neurotransmission in human cortex

Abstract Neuronal activity in the brain reflects an excitation–inhibition balance that is regulated predominantly by glutamatergic and GABAergic neurotransmission, and often disturbed in neuropsychiatric disorders. Here, we tested the effects of a single oral dose of two anti-glutamatergic drugs (de...

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Autores principales:	Paolo Belardinelli, Franca König, Chen Liang, Isabella Premoli, Debora Desideri, Florian Müller-Dahlhaus, Pedro Caldana Gordon, Carl Zipser, Christoph Zrenner, Ulf Ziemann
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7ef4d5033f584e31b11159a369683d7b
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spelling	oai:doaj.org-article:7ef4d5033f584e31b11159a369683d7b2021-12-02T15:51:14ZTMS-EEG signatures of glutamatergic neurotransmission in human cortex10.1038/s41598-021-87533-z2045-2322https://doaj.org/article/7ef4d5033f584e31b11159a369683d7b2021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-87533-zhttps://doaj.org/toc/2045-2322Abstract Neuronal activity in the brain reflects an excitation–inhibition balance that is regulated predominantly by glutamatergic and GABAergic neurotransmission, and often disturbed in neuropsychiatric disorders. Here, we tested the effects of a single oral dose of two anti-glutamatergic drugs (dextromethorphan, an NMDA receptor antagonist; perampanel, an AMPA receptor antagonist) and an L-type voltage-gated calcium channel blocker (nimodipine) on transcranial magnetic stimulation (TMS)-evoked electroencephalographic (EEG) potentials (TEPs) and TMS-induced oscillations (TIOs) in 16 healthy adults in a pseudorandomized, double-blinded, placebo-controlled crossover design. Single-pulse TMS was delivered to the hand area of left primary motor cortex. Dextromethorphan increased the amplitude of the N45 TEP, while it had no effect on TIOs. Perampanel reduced the amplitude of the P60 TEP in the non-stimulated hemisphere, and increased TIOs in the beta-frequency band in the stimulated sensorimotor cortex, and in the alpha-frequency band in midline parietal channels. Nimodipine and placebo had no effect on TEPs and TIOs. The TEP results extend previous pharmaco-TMS-EEG studies by demonstrating that the N45 is regulated by a balance of GABAAergic inhibition and NMDA receptor-mediated glutamatergic excitation. In contrast, AMPA receptor-mediated glutamatergic neurotransmission contributes to propagated activity reflected in the P60 potential and midline parietal induced oscillations. This pharmacological characterization of TMS-EEG responses will be informative for interpreting TMS-EEG abnormalities in neuropsychiatric disorders with pathological excitation–inhibition balance.Paolo BelardinelliFranca KönigChen LiangIsabella PremoliDebora DesideriFlorian Müller-DahlhausPedro Caldana GordonCarl ZipserChristoph ZrennerUlf ZiemannNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Paolo Belardinelli Franca König Chen Liang Isabella Premoli Debora Desideri Florian Müller-Dahlhaus Pedro Caldana Gordon Carl Zipser Christoph Zrenner Ulf Ziemann TMS-EEG signatures of glutamatergic neurotransmission in human cortex
description	Abstract Neuronal activity in the brain reflects an excitation–inhibition balance that is regulated predominantly by glutamatergic and GABAergic neurotransmission, and often disturbed in neuropsychiatric disorders. Here, we tested the effects of a single oral dose of two anti-glutamatergic drugs (dextromethorphan, an NMDA receptor antagonist; perampanel, an AMPA receptor antagonist) and an L-type voltage-gated calcium channel blocker (nimodipine) on transcranial magnetic stimulation (TMS)-evoked electroencephalographic (EEG) potentials (TEPs) and TMS-induced oscillations (TIOs) in 16 healthy adults in a pseudorandomized, double-blinded, placebo-controlled crossover design. Single-pulse TMS was delivered to the hand area of left primary motor cortex. Dextromethorphan increased the amplitude of the N45 TEP, while it had no effect on TIOs. Perampanel reduced the amplitude of the P60 TEP in the non-stimulated hemisphere, and increased TIOs in the beta-frequency band in the stimulated sensorimotor cortex, and in the alpha-frequency band in midline parietal channels. Nimodipine and placebo had no effect on TEPs and TIOs. The TEP results extend previous pharmaco-TMS-EEG studies by demonstrating that the N45 is regulated by a balance of GABAAergic inhibition and NMDA receptor-mediated glutamatergic excitation. In contrast, AMPA receptor-mediated glutamatergic neurotransmission contributes to propagated activity reflected in the P60 potential and midline parietal induced oscillations. This pharmacological characterization of TMS-EEG responses will be informative for interpreting TMS-EEG abnormalities in neuropsychiatric disorders with pathological excitation–inhibition balance.
format	article
author	Paolo Belardinelli Franca König Chen Liang Isabella Premoli Debora Desideri Florian Müller-Dahlhaus Pedro Caldana Gordon Carl Zipser Christoph Zrenner Ulf Ziemann
author_facet	Paolo Belardinelli Franca König Chen Liang Isabella Premoli Debora Desideri Florian Müller-Dahlhaus Pedro Caldana Gordon Carl Zipser Christoph Zrenner Ulf Ziemann
author_sort	Paolo Belardinelli
title	TMS-EEG signatures of glutamatergic neurotransmission in human cortex
title_short	TMS-EEG signatures of glutamatergic neurotransmission in human cortex
title_full	TMS-EEG signatures of glutamatergic neurotransmission in human cortex
title_fullStr	TMS-EEG signatures of glutamatergic neurotransmission in human cortex
title_full_unstemmed	TMS-EEG signatures of glutamatergic neurotransmission in human cortex
title_sort	tms-eeg signatures of glutamatergic neurotransmission in human cortex
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/7ef4d5033f584e31b11159a369683d7b
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TMS-EEG signatures of glutamatergic neurotransmission in human cortex

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