Thalamocortical Mechanisms for the Anteriorization of Alpha Rhythms during Propofol-Induced Unconsciousness

As humans are induced into a state of general anesthesia via propofol, the normal alpha rhythm (8–13 Hz) in the occipital cortex disappears and a frontal alpha rhythm emerges. This spatial shift in alpha activity is called anteriorization. We present a thalamocortical model that suggests mechanisms...

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Detalhes bibliográficos
Principais autores: Vijayan, Sujith, Purdon, Patrick Lee, Kopell, Nancy J., Ching, Shinung, Brown, Emery Neal
Outros Autores: Massachusetts Institute of Technology. Institute for Medical Engineering & Science
Formato: Artigo
Idioma:en_US
Publicado em: Society for Neuroscience 2014
Acesso em linha:http://hdl.handle.net/1721.1/89132
https://orcid.org/0000-0001-5651-5060
https://orcid.org/0000-0003-2668-7819
Descrição
Resumo:As humans are induced into a state of general anesthesia via propofol, the normal alpha rhythm (8–13 Hz) in the occipital cortex disappears and a frontal alpha rhythm emerges. This spatial shift in alpha activity is called anteriorization. We present a thalamocortical model that suggests mechanisms underlying anteriorization. Our model captures the neural dynamics of anteriorization when we adjust it to reflect two key actions of propofol: its potentiation of GABA and its reduction of the hyperpolarization-activated current I[subscript h]. The reduction in I[subscript h] abolishes the occipital alpha by silencing a specialized subset of thalamocortical cells, thought to generate occipital alpha at depolarized membrane potentials (>−60 mV). The increase in GABA inhibition imposes an alpha timescale on both the cortical and thalamic portions of the frontal component that are reinforced by reciprocal thalamocortical feedback. Anteriorization can thus be understood as a differential effect of anesthetic drugs on thalamic nuclei with disparate spatial projections, i.e.: (1) they disrupt the normal, depolarized alpha in posterior-projecting thalamic nuclei while (2) they engage a new, hyperpolarized alpha in frontothalamic nuclei. Our model generalizes to other anesthetics that include GABA as a target, since the molecular targets of many such anesthetics alter the model dynamics in a manner similar to that of propofol.