Characterization of cortical states is essential for understanding brain functioning in the absence of external stimuli. The balance between excitation and inhibition and the number of non-redundant activity patterns, indexed by the 1/f slope and LZc respectively, distinguish cortical states. However, the relation between these two measures has not been characterized. Here we analyzed the relation between 1/f slope and LZc with two modeling approaches and in empirical human EEG and monkey ECoG data. We contrasted resting state with propofol anesthesia, which is known to modulate the excitation-inhibition balance. We found convergent results among all strategies employed, showing an inverse and not trivial monotonic relation between 1/f slope and complexity. This behavior was observed even when the signals’ spectral properties were heavily manipulated, consistent at ECoG and EEG scales. Models also showed that LZc was strongly dependent on 1/f slope but independent of the signal’s spectral power law’s offset. Our results show that, although these measures have very distinct mathematical origins, they are closely related. We hypothesize that differentially entropic regimes could underlie the link between the excitation-inhibition balance and the vastness of repertoire of cortical systems.
Summary Mechanisms underlying loss of consciousness following propofol administration remain incompletely understood. The objective of this study was to compare frontal lobe electroencephalography activity and brainstem reflexes during intravenous induction of general anaesthesia, in patients receiving a typical bolus dose (fast infusion) of propofol compared with a slower infusion rate. We sought to determine whether brainstem suppression (‘bottom‐up’) predominates over loss of cortical function (‘top‐down’). Sixteen ASA physical status‐1 patients were randomly assigned to either a fast or slow propofol infusion group. Loss of consciousness and brainstem reflexes were assessed every 30 s by a neurologist blinded to treatment allocation. We performed a multitaper spectral analysis of all electroencephalography data obtained from each participant. Brainstem reflexes were present in all eight patients in the slow infusion group, while being absent in all patients in the fast infusion group, at the moment of loss of consciousness (p = 0.010). An increase in alpha band power was observed before loss of consciousness only in participants allocated to the slow infusion group. Alpha band power emerged several minutes after the loss of consciousness in participants allocated to the fast infusion group. Our results show a predominance of ‘bottom‐up’ mechanisms during fast infusion rates and ‘top‐down’ mechanisms during slow infusion rates. The underlying mechanisms by which propofol induces loss of consciousness are potentially influenced by the speed of infusion.
Hippocampal-dependent memories emerge late during postnatal development, aligning with hippocampal maturation. During sleep, the two-stage memory formation model states that through hippocampal-neocortical interactions, cortical slow-oscillations (SO), thalamocortical Spindles, and hippocampal sharp-wave ripples (SWR) are synchronized, allowing for the consolidation of hippocampal-dependent memories. However, evidence supporting this hypothesis during development is still lacking. Therefore, we performed successive object-in-place tests during a window of memory emergence and recorded in vivo the occurrence of SO, Spindles, and SWR during sleep, immediately after the memory encoding stage of the task. We found that hippocampal-dependent memory emerges at the end of the 4th postnatal week independently of task overtraining. Furthermore, we observed that those animals with better performance in the memory task had increased Spindle density and duration and lower density of SWR. Moreover, we observed changes in the SO-Spindle and Spindle-SWR temporal-coupling during this developmental period. Our results provide new evidence for the onset of hippocampal-dependent memory and its relationship to the oscillatory phenomenon occurring during sleep that helps us understand how memory consolidation models fit into the early stages of postnatal development.
Neural correlates of cognitive planning are not understood well at present. Behavioral paradigms targeting this function are a current challenge in cognitive neuroscience. We recorded EEG activity while subjects were performing a novel behavioral paradigm that evaluates cognitive planning function. Participants showed longer reaction times and decreased accuracy during the planning condition compared to the control condition, suggesting that the planning condition is more time consuming, therefore reflecting higher cognitive demand. Moreover, cognitive planning induced a frontal midline theta (FMθ) frequency band originating in prefrontal cortex (PFC) as shown in previous cognitive control studies. When subjects began planning, there was a progressive and sustained increase in FMθ starting after 500 milliseconds (ms) of planning. Hence, we characterized for first time, both spatial and temporal FMθ dynamics of cognitive planning as a marker of cognitive control function.
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