Marcello Massimini

ORCID iD
https://orcid.org/0000-0003-2271-957X
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Scopus Author ID: 6603479164

Sources:
Scopus - Elsevier (2015-09-29)

ResearcherID: T-8115-2017

Sources:
ResearcherID (2017-11-20)

Biography

My whole research activity, from the cellular level to the patient, has been devoted to understanding what changes in thalamocortical networks (in terms of spontaneous activity and connectivity patterns,) when consciousness fades and recovers. Hence, in order to understand the cellular mechanism of slow EEG oscillations of sleep and anesthesia, I carried out the simultaneous intracellular recording of cortical neurons, glial cells and extracellular calcium concentration in vivo (Massimini et al, J. Neurophysiol 2001; Amzica, Massimini, Cereb. Cortex 2002; Amzica, Massimini, J. Neurosc 2002). At the University of Wisconsin, in the lab of Dr. Giulio Tononi, I performed high-density EEG recordings (256 channels) in sleeping humans, which showed that sleep slow oscillations behave as traveling waves of neuronal hyperpolarization-depolarization (Massimini et al., J. Neurosci. 2005). Most important, I focused on the development and validation of a novel technique (TMS/hd-EEG), which enables studying directly cortico- cortical communication in humans. Employing this system I performed original experiments, which demonstrated that the fading of consciousness during NREM sleep is associated with a substantial impairment of the brain’s capacity to sustain complex intracortical communication (Massimini et al., Science 2005), possibly due to the bistable behavior of cortical neurons (Massimini et al., PNAS 2007; Tononi and Massimini, Proc. NY Acad. Sci., 2008). The link between sleep-like bistability, cortico-cortical communication and loss of consciousness was subsequently extended to other conditions by experiments performed during anesthesia (Ferrarelli, Massimini et al., PNAS 2010) and coma (Rosanova et al., Brain 2012; Casali et al., Science Translational Medicine 2013). Altogether, these works led me to investigate the general hypothesis that brain lesions may impair cortico-cortical information transmission, above and beyond the associated anatomical disconnection, by inducing bistability in portions of the thalamocortical system that are otherwise healthy (Massimini et al., AIB 2012; Sarasso et al., Clin. EEG Neurosci., 2014).
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