scholarly journals Neural signatures of loss of consciousness and its recovery by thalamic stimulation

2019 ◽  
Author(s):  
Jacob A. Donoghue ◽  
André M. Bastos ◽  
Jorge Yanar ◽  
Simon Kornblith ◽  
Meredith Mahnke ◽  
...  

AbstractWe know that general anesthesia produces unconsciousness but not quite how. We recorded neural activity from the frontal, parietal, and temporal cortices and thalamus while maintaining unconsciousness in non-human primates (NHPs) with propofol. Unconsciousness was marked by slow frequency (∼1 Hz) oscillations in local field potentials, entraining local spiking to Up states alternating with Down states of little spiking, and decreased higher frequency (>4 Hz) coherence. The thalamus contributed to cortical rhythms. Its stimulation “awakened” anesthetized NHPs and reversed the electrophysiologic features of unconsciousness. Unconsciousness thus resulted from slow frequency hypersynchrony and loss of high-frequency dynamics, partly mediated by the thalamus, that disrupts cortical communication/integration.

2020 ◽  
Author(s):  
André M. Bastos ◽  
Jacob A. Donoghue ◽  
Scott L. Brincat ◽  
Meredith Mahnke ◽  
Jorge Yanar ◽  
...  

AbstractThe specific circuit mechanisms through which anesthetics induce unconsciousness have not been completely characterized. We recorded neural activity from the frontal, parietal, and temporal cortices and thalamus while maintaining unconsciousness in non-human primates (NHPs) with the anesthetic propofol. Unconsciousness was marked by slow frequency (~1 Hz) oscillations in local field potentials, entrainment of local spiking to Up states alternating with Down states of little spiking, and decreased coherence in frequencies above 4 Hz. Thalamic stimulation “awakened” anesthetized NHPs and reversed the electrophysiologic features of unconsciousness. Unconsciousness is linked to cortical and thalamic slow frequency synchrony coupled with decreased spiking, and loss of higher-frequency dynamics. This may disrupt cortical communication/integration.


eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
André M Bastos ◽  
Jacob A Donoghue ◽  
Scott L Brincat ◽  
Meredith Mahnke ◽  
Jorge Yanar ◽  
...  

The specific circuit mechanisms through which anesthetics induce unconsciousness have not been completely characterized. We recorded neural activity from the frontal, parietal, and temporal cortices and thalamus while maintaining unconsciousness in non-human primates (NHPs) with the anesthetic propofol. Unconsciousness was marked by slow frequency (~1 Hz) oscillations in local field potentials, entrainment of local spiking to Up states alternating with Down states of little or no spiking activity, and decreased coherence in frequencies above 4 Hz. Thalamic stimulation ‘awakened’ anesthetized NHPs and reversed the electrophysiologic features of unconsciousness. Unconsciousness is linked to cortical and thalamic slow frequency synchrony coupled with decreased spiking, and loss of higher-frequency dynamics. This may disrupt cortical communication/integration.


Epilepsia ◽  
2015 ◽  
Vol 57 (1) ◽  
pp. 111-121 ◽  
Author(s):  
Shennan Aibel Weiss ◽  
Catalina Alvarado-Rojas ◽  
Anatol Bragin ◽  
Eric Behnke ◽  
Tony Fields ◽  
...  

Brain ◽  
2019 ◽  
Vol 142 (8) ◽  
pp. 2288-2302 ◽  
Author(s):  
Mahsa Malekmohammadi ◽  
Collin M Price ◽  
Andrew E Hudson ◽  
Jasmine A T DiCesare ◽  
Nader Pouratian

It is unclear how anaesthesia affects activity across brain networks. Using local field potentials recorded directly from the ventral intermediate nucleus of the thalamus and frontoparietal cortex in patients undergoing DBS surgery, Malekmohammadi et al. report the breakdown of α functional thalamocortical connectivity under propofol anaesthesia despite local power increases.


NeuroImage ◽  
2015 ◽  
Vol 114 ◽  
pp. 185-198 ◽  
Author(s):  
Ruggero G. Bettinardi ◽  
Núria Tort-Colet ◽  
Marcel Ruiz-Mejias ◽  
Maria V. Sanchez-Vives ◽  
Gustavo Deco

2020 ◽  
Author(s):  
Yusuke Watanabe ◽  
Mami Okada ◽  
Yuji Ikegaya

AbstractHippocampal ripples are transient neuronal features observed in high-frequency oscillatory bands of local field potentials, and they occur primarily during periods of behavioral immobility and slow-wave sleep. Ripples have been defined based on mathematically engineered features, such as magnitudes, durations, and cycles per event. However, the “ripples” could vary from laboratory to laboratory because their definition is subject to human bias, including the arbitrary choice of parameters and thresholds. In addition, local field potentials are often influenced by myoelectric noise arising from animal movement, making it difficult to distinguish ripples from high-frequency noises. To overcome these problems, we extracted ripple candidates under few constraints and labeled them as binary or stochastic “true” or “false” ripples using Gaussian mixed model clustering and a deep convolutional neural network in a weakly supervised fashion. Our automatic method separated ripples and myoelectric noise and was able to detect ripples even when the animals were moving. Moreover, we confirmed that a convolutional neural network was able to detect ripples defined by our method. Leave-one-animal-out cross-validation estimated the area under the precision-recall curve for ripple detection to be 0.72. Finally, our model establishes an appropriate threshold for the ripple magnitude in the case of the conventional detection of ripples.


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