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Genetic polymorphisms in COMT and BDNF influence synchronization dynamics of human neuronal oscillations

Neuronal oscillations, their inter-areal synchronization, and scale-free dynamics constitute fundamental mechanisms for cognition by regulating communication in neuronal networks. These oscillatory dynamics have large inter-individual variability that is partly heritable. We hypothesized that this v...

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Detalles Bibliográficos
Autores principales: Simola, Jaana, Siebenhühner, Felix, Myrov, Vladislav, Kantojärvi, Katri, Paunio, Tiina, Palva, J. Matias, Brattico, Elvira, Palva, Satu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9460523/
https://www.ncbi.nlm.nih.gov/pubmed/36093050
http://dx.doi.org/10.1016/j.isci.2022.104985
Descripción
Sumario:Neuronal oscillations, their inter-areal synchronization, and scale-free dynamics constitute fundamental mechanisms for cognition by regulating communication in neuronal networks. These oscillatory dynamics have large inter-individual variability that is partly heritable. We hypothesized that this variability could be partially explained by genetic polymorphisms in neuromodulatory genes. We recorded resting-state magnetoencephalography (MEG) from 82 healthy participants and investigated whether oscillation dynamics were influenced by genetic polymorphisms in catechol-O-methyltransferase (COMT) Val(158)Met and brain-derived neurotrophic factor (BDNF) Val(66)Met. Both COMT and BDNF polymorphisms influenced local oscillation amplitudes and their long-range temporal correlations (LRTCs), while only BDNF polymorphism affected the strength of large-scale synchronization. Our findings demonstrate that COMT and BDNF genetic polymorphisms contribute to inter-individual variability in neuronal oscillation dynamics. Comparison of these results to computational modeling of near-critical synchronization dynamics further suggested that COMT and BDNF polymorphisms influenced local oscillations by modulating the excitation-inhibition balance according to the brain criticality framework.