TMS- EEG Signatures of GABAergic Neurotransmission in the Human Cortex

Premoli, Isabella; Castellanos, Nazareth; Rivolta, Davide; Belardinelli, Paolo; Bajo Breton, Ricardo; Zipser, Carl; Espenhahn, Svenja; Heidegger, Tonio; Mueller-Dahlhaus, Florian y Ziemann, Ulf (2014). TMS- EEG Signatures of GABAergic Neurotransmission in the Human Cortex. "The Journal of Neuroscience", v. 34 (n. 16); pp. 5603-5612. ISSN 0270-6474. https://doi.org/10.1523/JNEUROSCI.5089-13.2014.

Descripción

Título: TMS- EEG Signatures of GABAergic Neurotransmission in the Human Cortex
Autor/es:
  • Premoli, Isabella
  • Castellanos, Nazareth
  • Rivolta, Davide
  • Belardinelli, Paolo
  • Bajo Breton, Ricardo
  • Zipser, Carl
  • Espenhahn, Svenja
  • Heidegger, Tonio
  • Mueller-Dahlhaus, Florian
  • Ziemann, Ulf
Tipo de Documento: Artículo
Título de Revista/Publicación: The Journal of Neuroscience
Fecha: 2014
Volumen: 34
Materias:
Palabras Clave Informales: Electroencephalography; GABA; human cortex; inhibition; pharmaco-TMS-EEG; transcranial magnetic stimulation
Escuela: E.T.S.I. Telecomunicación (UPM)
Departamento: Tecnología Fotónica [hasta 2014]
Licencias Creative Commons: Reconocimiento - Sin obra derivada - No comercial

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Resumen

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.

Más información

ID de Registro: 35624
Identificador DC: http://oa.upm.es/35624/
Identificador OAI: oai:oa.upm.es:35624
Identificador DOI: 10.1523/JNEUROSCI.5089-13.2014
URL Oficial: http://www.jneurosci.org/content/34/16/5603.full
Depositado por: Memoria Investigacion
Depositado el: 16 Jun 2015 17:01
Ultima Modificación: 01 Nov 2015 23:56
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