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Gamma oscillations in V1 are correlated with GABA(A) receptor density: A multi-modal MEG and Flumazenil-PET study.

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Titel: Gamma oscillations in V1 are correlated with GABA(A) receptor density: A multi-modal MEG and Flumazenil-PET study.
Autoren: Kujala, J., Jung, J., Bouvard, S., Lecaignard, F., Lothe, A., Bouet, R., Ciumas, C., Ryvlin, P., Jerbi, K.
Publikationsjahr: 2025
Bestand: Université de Lausanne (UNIL): Serval - Serveur académique lausannois
Schlagwörter: Adult, Female, Flumazenil/chemistry, Humans, Magnetic Resonance Imaging, Magnetoencephalography, Male, Positron-Emission Tomography, Receptors, GABA-A/metabolism, Visual Cortex/metabolism, gamma-Aminobutyric Acid/metabolism
Beschreibung: High-frequency oscillations in the gamma-band reflect rhythmic synchronization of spike timing in active neural networks. The modulation of gamma oscillations is a widely established mechanism in a variety of neurobiological processes, yet its neurochemical basis is not fully understood. Modeling, in-vitro and in-vivo animal studies suggest that gamma oscillation properties depend on GABAergic inhibition. In humans, search for evidence linking total GABA concentration to gamma oscillations has led to promising -but also to partly diverging- observations. Here, we provide the first evidence of a direct relationship between the density of GABA(A) receptors and gamma oscillatory gamma responses in human primary visual cortex (V1). By combining Flumazenil-PET (to measure resting-levels of GABA(A) receptor density) and MEG (to measure visually-induced gamma oscillations), we found that GABA(A) receptor densities correlated positively with the frequency and negatively with amplitude of visually-induced gamma oscillations in V1. Our findings demonstrate that gamma-band response profiles of primary visual cortex across healthy individuals are shaped by GABA(A)-receptor-mediated inhibitory neurotransmission. These results bridge the gap with in-vitro and animal studies and may have future clinical implications given that altered GABAergic function, including dysregulation of GABA(A) receptors, has been related to psychiatric disorders including schizophrenia and depression.
Publikationsart: article in journal/newspaper
Dateibeschreibung: application/pdf
Sprache: English
ISBN: 978-0-00-364788-4
0-00-364788-9
ISSN: 2045-2322
Relation: Scientific Reports; https://iris.unil.ch/handle/iris/153671; serval:BIB_BB277D188C2B; 000364788900001
DOI: 10.1038/srep16347
Verfügbarkeit: https://iris.unil.ch/handle/iris/153671
https://doi.org/10.1038/srep16347
Dokumentencode: edsbas.E5B81C2D
Datenbank: BASE
Beschreibung
Abstract:High-frequency oscillations in the gamma-band reflect rhythmic synchronization of spike timing in active neural networks. The modulation of gamma oscillations is a widely established mechanism in a variety of neurobiological processes, yet its neurochemical basis is not fully understood. Modeling, in-vitro and in-vivo animal studies suggest that gamma oscillation properties depend on GABAergic inhibition. In humans, search for evidence linking total GABA concentration to gamma oscillations has led to promising -but also to partly diverging- observations. Here, we provide the first evidence of a direct relationship between the density of GABA(A) receptors and gamma oscillatory gamma responses in human primary visual cortex (V1). By combining Flumazenil-PET (to measure resting-levels of GABA(A) receptor density) and MEG (to measure visually-induced gamma oscillations), we found that GABA(A) receptor densities correlated positively with the frequency and negatively with amplitude of visually-induced gamma oscillations in V1. Our findings demonstrate that gamma-band response profiles of primary visual cortex across healthy individuals are shaped by GABA(A)-receptor-mediated inhibitory neurotransmission. These results bridge the gap with in-vitro and animal studies and may have future clinical implications given that altered GABAergic function, including dysregulation of GABA(A) receptors, has been related to psychiatric disorders including schizophrenia and depression.
ISBN:9780003647884
0003647889
ISSN:20452322
DOI:10.1038/srep16347