Cortical functional connectivity indexes arousal state during sleep and anesthesia Abstract   Disruption of cortical connectivity likely contributes to loss of consciousness (LOC) during both sleep and general anesthesia, but the degree of overlap in the underlying mechanisms is unclear. Both sleep and anesthesia comprise states of varying levels of arousal and consciousness, including states of largely maintained conscious experience (sleep: N1, REM; anesthesia: sedated but responsive) as well as states of substantially reduced conscious experience (sleep: N2N3; anesthesia: unresponsive). Here, we tested the hypotheses that (1) cortical connectivity will exhibit clear changes when transitioning into states of reduced consciousness, and (2) these changes will be similar for arousal states of comparable levels of consciousness during sleep and anesthesia. Using intracranial recordings from five adult neurosurgical patients, we compared resting state cortical functional connectivity (as measured by weighted phase lag index, wPLI) in the same subjects across arousal states during natural sleep wake (WS), N1, N2, N3, REM and propofol anesthesia predrug wake (WA), sedatedresponsive (S), and unresponsive (U). Analysis of alphaband connectivity indicated a transition boundary distinguishing states of maintained and reduced conscious experience in both sleep and anesthesia. In wake states WS and WA, alphaband wPLI within the temporal lobe was dominant. This pattern was largely unchanged in N1, REM, and S. Transitions into states of reduced consciousness N2, N3, and U were characterized by dramatic changes in connectivity, with dominant connections shifting to prefrontal cortex. Secondary analyses indicated similarities in reorganization of cortical connectivity in sleep and anesthesia. Shifts from temporal to frontal cortical connectivity may reflect impaired sensory processing in states of reduced consciousness. The data indicate that functional connectivity can serve as a biomarker of arousal state and suggest common mechanisms of LOC in sleep and anesthesia.

Interactions between stimulievoked cortical activity and spontaneous low frequency oscillations measured with neuronal calcium Abstract   Spontaneous brain activity has been widely used to map brain connectivity. The interactions between taskevoked brain responses and the spontaneous cortical oscillations, especially within the low frequency range of xe2x88xbc0.1xe2x80xafHz, are not fully understood. Trialtotrial variabilities in brainu0027s response to sensory stimuli and the ability for brain to detect under noisy conditions suggest an appreciable impact of the brain state. Using a multimodality imaging platform, we simultaneously imaged neuronal Ca2 and cerebral hemodynamics at baseline and in response to singlepulse forepaw stimuli in ratu0027s somatosensory cortex. The high sensitivity of this system enables detection of responses to very weak and strong stimuli and real time determination of low frequency oscillations without averaging. Results show that the ongoing neuronal oscillations inversely modulate Ca2 transients evoked by sensory stimuli. High intensity stimuli reset the spontaneous neuronal oscillations to an unpreferable excitability following the stimulus. Cerebral hemodynamic responses also inversely interact with the spontaneous hemodynamic oscillations, correlating with the neuronal Ca2 transient changes. The results reveal competing interactions between spontaneous oscillations and stimulationevoked brain activities in somatosensory cortex and the resultant hemodynamics.