CompNet, Boston University Center for Computational Neuroscience and Neural Technology CompNet, Boston University Center for Computational Neuroscience and Neural Technology

CNS Alumni Colloquium by Levin Kuhlmann

CNS Graduate Levin Kuhlmann will be giving a CNS Alumni Colloquium on Friday the 19th, at 2:00 in the CompNet Building. See below for event details.

Event Details

CompNet cordially invites you to attend Dr. Kuhlmann's presentation of his research at the CNS Alumni Colloquium.

Agent Invariant Network Changes Leading to Drug Induced Unconsciousness
by Dr. Levin Kuhlmann

Brain Dynamics Research Unit
Brain & Psychological Sciences Research Centre
Swinburne University of Technology
Hawthorn VIC 3122, Australia

NeuroEngineering Laboratory
Department of Electrical and Electronic Engineering
The University of Melbourne
Parkville VIC 3010, Australia

Boston University
Friday, October 19th, 2012
2:00 p.m.
CompNet Building
Auditorium - Basement Room B03
677 Beacon Street
Boston, Massachusetts

A reception will immediately follow the colloquium.

Abstract

Parietal networks play a central role in the cortical information synthesis that supports conscious experience and behavior. Significant reductions in parietal level functional connectivity have been shown to occur during general anesthesia with propofol and a range of other GABAergic general anesthetic agents. Using two analysis approaches (1) a graph theoretic analysis based on surrogate-corrected zero-lag correlations of scalp EEG, and (2) a global coherence analysis based on the EEG cross-spectrum, we reveal that sedation with the NMDA antagonist nitrous oxide, an agent that has quite different electroencephalographic effects compared to the inductive general anesthetics, also causes significant alterations in parietal level functional networks, as well as changes in full brain and frontal level networks. Nitrous oxide-induced reductions in parietal network level functional connectivity were exclusively detected by utilising a surface Laplacian derivation, suggesting that superficial, smaller spatial scale, cortical networks were most affected. In contrast reductions in frontal network functional connectivity were optimally discriminated using a common-reference derivation, indicating that the NMDA antagonist nitrous oxide induces spatially coherent and widespread perturbations in frontal activity. Our findings not only give important weight to the idea of agent invariant, final network changes leading to drug induced unconsciousness, but also provide significant impetus for the application and development of multiscale functional analyses to systematically characterise the network level cortical effects of NMDA-related hypofunction.