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  TMS-EEG signatures of GABAergic neurotransmission in the human cortex

Premoli, I., Castellanos, N., Rivolta, D., Belardinelli, P., Bajo, R., Zipser, C., et al. (2014). TMS-EEG signatures of GABAergic neurotransmission in the human cortex. The Journal of Neuroscience, 34(16), 5603-5612. doi:10.1523/JNEUROSCI.5089-13.2014.

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Item Permalink: https://hdl.handle.net/11858/00-001M-0000-0024-E294-4 Version Permalink: https://hdl.handle.net/21.11116/0000-000B-6286-F
Genre: Journal Article

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2014
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Copyright © 2014 the authors
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https://www.jneurosci.org/content/34/16/5603 (Publisher version)
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 Creators:
Premoli, Isabella, Author
Castellanos, Nazareth, Author
Rivolta, Davide1, 2, Author
Belardinelli, Paolo, Author
Bajo, Ricardo, Author
Zipser, Carl, Author
Espenhahn, Svenja, Author
Heidegger, Tonio, Author
Müller-Dahlhaus, Florian, Author
Ziemann, Ulf, Author
Affiliations:
1Ernst Strüngmann Institute (ESI) for Neuroscience in Cooperation with Max Planck Society, Max Planck Society, Deutschordenstr. 46, 60528 Frankfurt, DE, ou_2074314              
2Singer Lab, Ernst Strüngmann Institute (ESI) for Neuroscience in Cooperation with Max Planck Society, Max Planck Society, Deutschordenstraße 46, 60528 Frankfurt, DE, ou_3381220              

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Free keywords: electroencephalography; GABA; human cortex; inhibition; pharmaco-TMS-EEG; transcranial magnetic stimulation
 Abstract: Combining transcranial magnetic stimulation (TMS) and electroencephalography (EEG) constitutes a powerful tool to directly assess human cortical excitability and connectivity. TMS of the primary motor cortex elicits a sequence of TMS-evoked EEG potentials (TEPs). It is thought that inhibitory neurotransmission through GABA-A receptors (GABAAR) modulates early TEPs (<50 ms after TMS), whereas GABA-B receptors (GABABR) play a role for later TEPs (at ∼100 ms after TMS). However, the physiological underpinnings of TEPs have not been clearly elucidated yet. Here, we studied the role of GABAA/B-ergic neurotransmission for TEPs in healthy subjects using a pharmaco-TMS-EEG approach. In Experiment 1, we tested the effects of a single oral dose of alprazolam (a classical benzodiazepine acting as allosteric-positive modulator at α1, α2, α3, and α5 subunit-containing GABAARs) and zolpidem (a positive modulator mainly at the α1 GABAAR) in a double-blind, placebo-controlled, crossover study. In Experiment 2, we tested the influence of baclofen (a GABABR agonist) and diazepam (a classical benzodiazepine) versus placebo on TEPs. Alprazolam and diazepam increased the amplitude of the negative potential at 45 ms after stimulation (N45) and decreased the negative component at 100 ms (N100), whereas zolpidem increased the N45 only. In contrast, baclofen specifically increased the N100 amplitude. These results provide strong evidence that the N45 represents activity of α1-subunit-containing GABAARs, whereas the N100 represents activity of GABABRs. Findings open a novel window of opportunity to study alteration of GABAA-/GABAB-related inhibition in disorders, such as epilepsy or schizophrenia.

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 Dates: 2014-04-162014
 Publication Status: Issued
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 Rev. Type: Peer
 Identifiers: DOI: 10.1523/JNEUROSCI.5089-13.2014
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Title: The Journal of Neuroscience
Source Genre: Journal
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Pages: - Volume / Issue: 34 (16) Sequence Number: - Start / End Page: 5603 - 5612 Identifier: -