Changes in the thalamocortical connectivity during anesthesia-induced transitions in consciousness.
Thalamocortical networks play an important role in information integration during consciousness. However, little is known about how the information flows between the thalamus and the cortex are affected by a loss of consciousness. To investigate this issue, we analyzed effective connectivity between the cortex and the thalamus in animals during anesthesia-induced transitions. By recording the electroencephalogram from the primary motor and the primary somatosensory cortex and by recording local field potentials from the ventral lateral and the ventrobasal thalamic nuclei, we evaluated changes in the conditional Granger causality between cortical and thalamic electrical activity as mice gradually lost consciousness from the use of anesthesia (ketamine/xylazine). The point of loss of consciousness was indicated by a moment of loss of movement that was measured using a head-mounted motion sensor. The results showed that 65% of the thalamocortical information flows were changed by anesthesia-induced loss of consciousness. Specifically, the effective connectivity between the cortex and the ventral lateral thalamus was altered such that the primary motor and the primary somatosensory cortex Granger-caused the ventral lateral thalamus before loss of consciousness whereas the ventral lateral thalamus Granger-caused the primary motor cortex and the primary somatosensory cortex after loss of consciousness. In contrast, the primary somatosensory cortex consistently Granger-caused the ventrobasal thalamus, regardless of the loss of consciousness. These results suggest how information flows change across the thalamocortical network during transitions in consciousness.
Department of Brain and Cognitive Engineering, Korea University, Seoul, Republic of Korea.
Sung-Phil
SP
Kim
Eunjin
E
Hwang
Jae-Hwan
JH
Kang
Seunghwan
S
Kim
Jee Hyun
JH
Choi
D000778:Anesthetics, Dissociative / Q000494:pharmacology*; D000818:Animals; D003243:Consciousness / Q000187:drug effects* / Q000502:physiology; D004569:Electroencephalography; D006993:Hypnotics and Sedatives / Q000494:pharmacology*; D007649:Ketamine / Q000494:pharmacology; D008297:Male; D051379:Mice; D009044:Motor Cortex / Q000187:drug effects* / Q000502:physiology; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D013003:Somatosensory Cortex / Q000187:drug effects* / Q000502:physiology; D013787:Thalamic Nuclei / Q000187:drug effects / Q000502:physiology; D014474:Unconsciousness / Q000139:chemically induced* / Q000503:physiopathology; D020651:Ventral Thalamic Nuclei / Q000187:drug effects / Q000502:physiology; D014991:Xylazine / Q000494:pharmacology
D000778:Anesthetics, Dissociative; D006993:Hypnotics and Sedatives; D014991:Xylazine; D007649:Ketamine