TY - JOUR TI - Disruption of thalamic functional connectivity is a neural correlate of dexmedetomidine-induced unconsciousness AU - Akeju, Oluwaseun AU - Loggia, Marco L AU - Catana, Ciprian AU - Pavone, Kara J AU - Vazquez, Rafael AU - Rhee, James AU - Contreras Ramirez, Violeta AU - Chonde, Daniel B AU - Izquierdo-Garcia, David AU - Arabasz, Grae AU - Hsu, Shirley AU - Habeeb, Kathleen AU - Hooker, Jacob M AU - Napadow, Vitaly AU - Brown, Emery N AU - Purdon, Patrick L A2 - Culham, Jody C VL - 3 PY - 2014 DA - 2014/11/28 SP - e04499 C1 - eLife 2014;3:e04499 DO - 10.7554/eLife.04499 UR - https://doi.org/10.7554/eLife.04499 AB - Understanding the neural basis of consciousness is fundamental to neuroscience research. Disruptions in cortico-cortical connectivity have been suggested as a primary mechanism of unconsciousness. By using a novel combination of positron emission tomography and functional magnetic resonance imaging, we studied anesthesia-induced unconsciousness and recovery using the α2-agonist dexmedetomidine. During unconsciousness, cerebral metabolic rate of glucose and cerebral blood flow were preferentially decreased in the thalamus, the Default Mode Network (DMN), and the bilateral Frontoparietal Networks (FPNs). Cortico-cortical functional connectivity within the DMN and FPNs was preserved. However, DMN thalamo-cortical functional connectivity was disrupted. Recovery from this state was associated with sustained reduction in cerebral blood flow and restored DMN thalamo-cortical functional connectivity. We report that loss of thalamo-cortical functional connectivity is sufficient to produce unconsciousness. KW - dexmedetomidine KW - consciousness KW - default mode network KW - thalamo-cortical KW - cortico-cortical KW - functional connectivity JF - eLife SN - 2050-084X PB - eLife Sciences Publications, Ltd ER -