scholarly journals Broadband slow-wave modulation in posterior and anterior cortex tracks distinct states of propofol-induced unconsciousness

2019 ◽  
Author(s):  
Emily P. Stephen ◽  
Gladia C. Hotan ◽  
Eric T. Pierce ◽  
P. Grace Harrell ◽  
John L. Walsh ◽  
...  
Keyword(s):  
Frontal Cortex ◽  
Slow Wave ◽  
Time Course ◽  
Wave Activity ◽  
Slow Waves ◽  
Brain State ◽  
Posterior Cortex ◽  
Anterior Cortex ◽  
Wave Modulation ◽  
Up And Down States

A controversy 5 has developed in recent years over the role that frontal and posterior cortices play in mediating consciousness and unconsciousness. One hypothesis proposes that posterior sensory and association cortices are the principal mediators of consciousness, citing evidence that strong slow-wave activity over posterior cortex during sleep disrupts the contents of dreaming. A competing hypothesis proposes that frontal-posterior interactions are critical to ignite a conscious percept, since activation of frontal cortex appears necessary for perception and can reverse unconsciousness under anesthesia. In both cases, EEG slow-waves (< 1 Hz) are considered evidence that up- and down-states are disrupting cortical activity necessary for consciousness. Here, we used anesthesia to study the interaction between the slow-wave and higher frequency activity in humans. If slow-waves are derived from underlying up and down-states, then they should modulate activity across a broad range of frequencies. We found that this broadband slow-wave modulation does occur: broadband slow-wave modulation occurs over posterior cortex when subjects initially become unconscious, but later encompasses both frontal and posterior cortex when subjects are more deeply anesthetized and likely unarousable. Based on these results, we argue that unconsciousness under anesthesia comprises several shifts in brain state that disrupt the sensory contents of consciousness distinct from arousal and awareness of those contents.Significance StatementThe roles of frontal and posterior cortices in mediating consciousness and unconsciousness are controversial. Disruption of posterior cortex during sleep appears to suppress the contents of dreaming, yet activation of frontal cortex appears necessary for perception and can reverse unconsciousness under anesthesia. We studied the time course of regional cortical disruption, as mediated by slow-wave modulation of broadband activity, during anesthesia-induced unconsciousness in humans. We found that broadband slow-wave modulation covered posterior cortex when subjects initially became unconscious, but later encompassed both frontal and posterior cortex when subjects were deeply anesthetized and likely unarousable. This suggests that unconsciousness under anesthesia comprises several shifts in brain state that disrupt the contents of consciousness distinct from arousal and awareness of those contents.

Slow Wave Activity Related to Working Memory Maintenance in the N-Back Task

2016 ◽  
Vol 30 (4) ◽  
pp. 141-154 ◽  
Author(s):  
Kira Bailey ◽  
Gregory Mlynarczyk ◽  
Robert West
Keyword(s):  
Working Memory ◽  
Slow Wave ◽  
Time Course ◽  
Relevant Information ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Response Accuracy ◽  
Functional Neuroanatomy ◽  
Stimulus Interval ◽  
Back Task

Abstract. Working memory supports our ability to maintain goal-relevant information that guides cognition in the face of distraction or competing tasks. The N-back task has been widely used in cognitive neuroscience to examine the functional neuroanatomy of working memory. Fewer studies have capitalized on the temporal resolution of event-related brain potentials (ERPs) to examine the time course of neural activity in the N-back task. The primary goal of the current study was to characterize slow wave activity observed in the response-to-stimulus interval in the N-back task that may be related to maintenance of information between trials in the task. In three experiments, we examined the effects of N-back load, interference, and response accuracy on the amplitude of the P3b following stimulus onset and slow wave activity elicited in the response-to-stimulus interval. Consistent with previous research, the amplitude of the P3b decreased as N-back load increased. Slow wave activity over the frontal and posterior regions of the scalp was sensitive to N-back load and was insensitive to interference or response accuracy. Together these findings lead to the suggestion that slow wave activity observed in the response-to-stimulus interval is related to the maintenance of information between trials in the 1-back task.

Effect of cromakalim and lemakalim on slow waves and membrane currents in colonic smooth muscle

1991 ◽  
Vol 260 (2) ◽  
pp. C375-C382 ◽  
Author(s):  
J. M. Post ◽  
R. J. Stevens ◽  
K. M. Sanders ◽  
J. R. Hume
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Slow Wave ◽  
Outward Current ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Ca Current ◽  
K Current ◽  
Stimulation Of

The effects of cromakalim (BRL 34915) and its optical isomer lemakalim (BRL 38227) were investigated in intact tissue and freshly dispersed circular muscle cells from canine proximal colon. Cromakalim and lemakalim hyperpolarized resting membrane potential, shortened the duration of slow waves by abolishing the plateau phase, and decreased the frequency of slow waves. Glyburide, a K channel blocker, prevented the effect of cromakalim on slow-wave activity. The mechanisms of these alterations in slow-wave activity were studied in isolated myocytes under voltage-clamp conditions. Cromakalim and lemakalim increased the magnitude of a time-independent outward K current, but cromakalim also reduced the peak outward K current. Glyburide inhibited lemakalim stimulation of the time-independent background current. Nisoldipine also reduced the peak outward current, and in the presence of nisoldipine, cromakalim did not affect the peak outward component of current. This suggested that cromakalim may block a Ca-dependent component of the outward current. Lemakalim did not affect the peak outward current. We tested whether the effects of cromakalim on outward current might be indirect due to an effect on inward Ca current. Cromakalim, but not lemakalim, was found to inhibit L-type Ca channels; however, glyburide did not alter cromakalim inhibition of inward Ca current. We conclude that the effects of cromakalim and lemakalim on membrane potential and slow waves in colonic smooth muscle appear to result primarily from stimulation of a time-independent background K conductance. The effects of these compounds on channel activity may explain the inhibitory effect of these compounds on contractile activity.

Selective lesioning of interstitial cells of Cajal by methylene blue and light leads to loss of slow waves

1994 ◽  
Vol 266 (3) ◽  
pp. G485-G496 ◽  
Author(s):  
L. W. Liu ◽  
L. Thuneberg ◽  
J. D. Huizinga
Keyword(s):  
Methylene Blue ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Electrical Activity ◽  
Slow Wave ◽  
Interstitial Cells Of Cajal ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Cells Of Cajal

Incubation with 50 microM methylene blue (MB) and subsequent intense illumination resulted in abolition of the slow-wave activity in the submuscular interstitial cells of Cajal-circular muscle (ICC-CM) preparations of canine colon. This was often accompanied by a decrease in resting membrane potential. Repolarization of cells back to -70 mV did not restore the slow-wave activity, indicating that MB plus light directly interrupted the generation mechanism of slow waves. After MB incubation, a 2-min illumination consistently changed the mitochondrial conformation in ICCs from very condensed to orthodox, without inducing any obvious changes in smooth muscle cells. After 4- to 10-min illumination, ICCs became progressively more damaged with swollen and ruptured mitochondria, loss of cytoplasmic contrast and detail, loss of caveolae, and rupture of the plasma membrane. No damage was seen in smooth muscle cells or nerves. Gap junctional ultrastructure was preserved. Intense illumination without preincubation with MB left the slow waves and the ultrastructure of ICC-CM preparations unaffected. In CM preparations, without the submuscular ICC-smooth-muscle network, MB plus light induced no changes in electrical activity. We conclude that the correlation between selective damage to the submuscular ICCs (relative to smooth muscle) and selective loss of the slow-wave activity (relative to other electrical activity of the CM) strongly indicates that the ICCs play an essential role in the generation of slow waves.

Quantitative cellular description of gastric slow wave activity

2008 ◽  
Vol 294 (4) ◽  
pp. G989-G995 ◽  
Author(s):  
Alberto Corrias ◽  
Martin L. Buist
Keyword(s):  
Slow Wave ◽  
Interstitial Cells Of Cajal ◽  
Quantitative Description ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Good Correspondence ◽  
Gastric Slow Wave ◽  
Intracellular Ca ◽  
Cells Of Cajal

Interstitial cells of Cajal (ICC) are responsible for the spontaneous and omnipresent electrical activity in the stomach. A quantitative description of the intracellular processes whose coordinated activity is believed to generate electrical slow waves has been developed and is presented here. In line with recent experimental evidence, the model describes how the interplay between the mitochondria and the endoplasmic reticulum in cycling intracellular Ca2+ provides the primary regulatory signal for the initiation of the slow wave. The major ion channels that have been identified as influencing slow wave activity have been modeled according to data obtained from isolated ICC. The model has been validated by comparing the simulated profile of the slow waves with experimental recordings and shows good correspondence in terms of frequency, amplitude, and shape in both control and pharmacologically altered conditions.

Menstrual Respiratory Changes and Symptoms

1980 ◽  
Vol 136 (5) ◽  
pp. 492-497 ◽  
Author(s):  
J. Damas-Mora ◽  
Lisa Davies ◽  
Wendy Taylor ◽  
F. A. Jenner
Keyword(s):  
Carbon Dioxide ◽  
Menstrual Cycle ◽  
Slow Wave ◽  
Respiratory System ◽  
Normal Subjects ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Premenstrual Tension ◽  
Carbon Dioxide Sensitivity

SummaryThe duration of standardised overbreathing required to produce slow wave activity in the EEG during different phases of the menstrual cycle has been studied, and changes in carbon dioxide sensitivity of the respiratory system. Normal subjects developed slow waves more quickly and had more sensitive CO2 responses during the premenstrual/menstrual phases. This may be a factor contributing to premenstrual tension.

Electrical slow-wave activity from the circular layer of cat terminal antrum

1991 ◽  
Vol 261 (1) ◽  
pp. G78-G82
Author(s):  
L. M. Renzetti ◽  
M. B. Wang ◽  
J. P. Ryan
Keyword(s):  
Slow Wave ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Muscle Layer ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Plateau Phase ◽  
Circular Layer ◽  
Upstroke Velocity

Intracellular recording techniques were used to characterize the electrical slow-wave activity through the thickness of the circular muscle layer of the cat terminal antrum. Muscle strips were pinned out in cross section to the floor of a recording chamber perfused with Krebs buffer. Circular muscle cells from the myenteric to the submucosal border then were impaled with 20- to 40-M omega glass microelectrodes, and slow-wave activity was recorded. Slow waves from the myenteric side of the circular layer consisted of an upstroke depolarization, a prominent plateau phase, and a downstroke repolarization. Slow-wave characteristics for cells along the myenteric border were Em, -74.2 +/- 1.3 mV; duration, 5.3 +/- 0.5 s; upstroke amplitude, 29.4 +/- 3.4 mV; upstroke velocity, 0.20 +/- 0.03 V/s; and frequency, 5.8 +/- 0.5/min. Slow waves from muscle cells along the submucosal side of the preparation lacked a discernible plateau phase. Slow waves from submucosal border cells had the following characteristics: Em, -80.4 +/- 1.4 mV (P less than 0.01); duration, 3.5 +/- 0.4 s (P less than 0.01); upstroke amplitude, 44.0 +/- 2.4 mV (P less than 0.01); upstroke velocity, 0.56 +/- 0.06 V/s (P less than 0.01); and frequency, 4.2 +/- 0.4/min (P less than 0.05). Slow waves were not affected by 10(-7)M tetrodotoxin and 10(-6)M atropine or by removal of the longitudinal muscle layer. Slow-wave activity within each region was maintained after dissecting the circular layer into submucosal and myenteric segments. The results suggest that two distinct slow waves exist within the circular muscle layer of the cat terminal antrum.(ABSTRACT TRUNCATED AT 250 WORDS)

Slow potential variations of small intestine

1961 ◽  
Vol 201 (1) ◽  
pp. 203-208 ◽  
Author(s):  
Alex Bortoff
Keyword(s):  
Small Intestine ◽  
Slow Wave ◽  
Time Course ◽  
Longitudinal Muscle ◽  
Time Derivative ◽  
Slow Waves ◽  
Slow Potential ◽  
True Time ◽  
Wave Discharge ◽  
Core Conductor

The various configurations of externally recorded slow waves from the small intestine of the cat are compared to those recorded intracellularly. It is shown that the slow waves represent periodic depolarizations of longitudinal muscle cells and that the flow of current associated with these depolarizations is similar to that in a core conductor. By recording monopolarly from a segment of intestine immersed in a volume conductor, slow waves are obtained having configurations ranging from those approximating the true time course and polarity of the intracellular slow wave to those approximating its second time derivative. This is shown to be a function of the pressure exerted by the electrode on the tissue. From a consideration of these results, plus those recently obtained by others, it is suggested that both "propagation" and synchronization of slow waves are manifestations of a modulation of slow wave discharge brought about either by electrotonic spread of current via low resistance intercellular pathways, or by voltage field effects.

Sleep homeostasis in the rat: Simulation of the time course of EEG slow-wave activity

1991 ◽  
Vol 130 (2) ◽  
pp. 141-144 ◽  
Author(s):  
Paul Franken ◽  
Irene Tobler ◽  
Alexander A. Borbély
Keyword(s):  
Slow Wave ◽  
Time Course ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Sleep Homeostasis

scholarly journals Pilot Study of Propofol-induced Slow Waves as a Pharmacologic Test for Brain Dysfunction after Brain Injury

2017 ◽  
Vol 126 (1) ◽  
pp. 94-103 ◽  
Author(s):  
Jukka Kortelainen ◽  
Eero Väyrynen ◽  
Usko Huuskonen ◽  
Jouko Laurila ◽  
Juha Koskenkari ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Brain Injury ◽  
Pilot Study ◽  
Slow Wave ◽  
Low Frequency ◽  
Brain Dysfunction ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Neurologic Outcome

Abstract Background Slow waves (less than 1 Hz) are the most important electroencephalogram signatures of nonrapid eye movement sleep. While considered to have a substantial importance in, for example, providing conditions for single-cell rest and preventing long-term neural damage, a disturbance in this neurophysiologic phenomenon is a potential indicator of brain dysfunction. Methods Since, in healthy individuals, slow waves can be induced with anesthetics, the authors tested the possible association between hypoxic brain injury and slow-wave activity in comatose postcardiac arrest patients (n = 10) using controlled propofol exposure. The slow-wave activity was determined by calculating the low-frequency (less than 1 Hz) power of the electroencephalograms recorded approximately 48 h after cardiac arrest. To define the association between the slow waves and the potential brain injury, the patients’ neurologic recovery was then followed up for 6 months. Results In the patients with good neurologic outcome (n = 6), the low-frequency power of electroencephalogram representing the slow-wave activity was found to substantially increase (mean ± SD, 190 ± 83%) due to the administration of propofol. By contrast, the patients with poor neurologic outcome (n = 4) were unable to generate propofol-induced slow waves. Conclusions In this experimental pilot study, the comatose postcardiac arrest patients with poor neurologic outcome were unable to generate normal propofol-induced electroencephalographic slow-wave activity 48 h after cardiac arrest. The finding might offer potential for developing a pharmacologic test for prognostication of brain injury by measuring the electroencephalographic response to propofol.

Sign in / Sign up

Export Citation Format

Share Document