Journal articles: 'Slow-wave oscillations'

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Mölle, Matthias, Oxana Yeshenko, Lisa Marshall, Susan J. Sara, and Jan Born. "Hippocampal Sharp Wave-Ripples Linked to Slow Oscillations in Rat Slow-Wave Sleep." Journal of Neurophysiology 96, no. 1 (July 2006): 62–70. http://dx.doi.org/10.1152/jn.00014.2006.

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Slow oscillations originating in the prefrontal neocortex during slow-wave sleep (SWS) group neuronal network activity and thereby presumably support the consolidation of memories. Here, we investigated whether the grouping influence of slow oscillations extends to hippocampal sharp wave-ripple (SPW) activity thought to underlie memory replay processes during SWS. The prefrontal surface EEG and multiunit activity (MUA), along with hippocampal local field potentials (LFP) from CA1, were recorded in rats during sleep. Average spindle and ripple activity and event correlation histograms of SPWs were calculated, time-locked to half-waves of slow oscillations. Results confirm decreased prefrontal MUA and spindle activity during EEG slow oscillation negativity and increases in this activity during subsequent positivity. A remarkably close temporal link was revealed between slow oscillations and hippocampal activity, with ripple activity and SPWs being also distinctly decreased during negative half-waves and increased during slow oscillation positivity. Fine-grained analyses of temporal dynamics revealed for the slow oscillation a phase delay of approximately 90 ms with reference to up and down states of prefrontal MUA, and of only approximately 60 ms with reference to changes in SPWs, indicating that up and down states in prefrontal MUA precede corresponding changes in hippocampal SPWs by approximately 30 ms. Results support the notion that the depolarizing surface-positive phase of the slow oscillation and the associated up state of prefrontal excitation promotes hippocampal SPWs via efferent pathways. The preceding disfacilitation of hippocampal events temporally coupled to the negative slow oscillation half-wave appears to serve a synchronizing role in this neocorticohippocampal interplay.

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Nakariakov, Valery M., and Dmitrii Y. Kolotkov. "Magnetohydrodynamic Waves in the Solar Corona." Annual Review of Astronomy and Astrophysics 58, no. 1 (August 18, 2020): 441–81. http://dx.doi.org/10.1146/annurev-astro-032320-042940.

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The corona of the Sun is a unique environment in which magnetohydrodynamic (MHD) waves, one of the fundamental processes of plasma astrophysics, are open to a direct study. There is striking progress in both observational and theoretical research of MHD wave processes in the corona, with the main recent achievements summarized as follows: ▪ Both periods and wavelengths of the principal MHD modes of coronal plasma structures, such as kink, slow and sausage modes, are confidently resolved. ▪ Scalings of various parameters of detected waves and waveguiding plasma structures allow for the validation of theoretical models. In particular, kink oscillation period scales linearly with the length of the oscillating coronal loop, clearly indicating that they are eigenmodes of the loop. Damping of decaying kink and standing slow oscillations depends on the oscillation amplitudes, demonstrating the importance of nonlinear damping. ▪ The dominant excitation mechanism for decaying kink oscillations is associated with magnetized plasma eruptions. Propagating slow waves are caused by the leakage of chromospheric oscillations. Fast wave trains could be formed by waveguide dispersion. ▪ The knowledge gained in the study of coronal MHD waves provides ground for seismological probing of coronal plasma parameters, such as the Alfvén speed, the magnetic field and its topology, stratification, temperature, fine structuring, polytropic index, and transport coefficients.

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Mizrahi-Kliger, Aviv D., Alexander Kaplan, Zvi Israel, and Hagai Bergman. "Desynchronization of slow oscillations in the basal ganglia during natural sleep." Proceedings of the National Academy of Sciences 115, no. 18 (April 16, 2018): E4274—E4283. http://dx.doi.org/10.1073/pnas.1720795115.

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Slow oscillations of neuronal activity alternating between firing and silence are a hallmark of slow-wave sleep (SWS). These oscillations reflect the default activity present in all mammalian species, and are ubiquitous to anesthesia, brain slice preparations, and neuronal cultures. In all these cases, neuronal firing is highly synchronous within local circuits, suggesting that oscillation–synchronization coupling may be a governing principle of sleep physiology regardless of anatomical connectivity. To investigate whether this principle applies to overall brain organization, we recorded the activity of individual neurons from basal ganglia (BG) structures and the thalamocortical (TC) network over 70 full nights of natural sleep in two vervet monkeys. During SWS, BG neurons manifested slow oscillations (∼0.5 Hz) in firing rate that were as prominent as in the TC network. However, in sharp contrast to any neural substrate explored thus far, the slow oscillations in all BG structures were completely desynchronized between individual neurons. Furthermore, whereas in the TC network single-cell spiking was locked to slow oscillations in the local field potential (LFP), the BG LFP exhibited only weak slow oscillatory activity and failed to entrain nearby cells. We thus show that synchrony is not inherent to slow oscillations, and propose that the BG desynchronization of slow oscillations could stem from its unique anatomy and functional connectivity. Finally, we posit that BG slow-oscillation desynchronization may further the reemergence of slow-oscillation traveling waves from multiple independent origins in the frontal cortex, thus significantly contributing to normal SWS.

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Jaar, Olivier, Mathieu Pilon, Julie Carrier, Jacques Montplaisir, and Antonio Zadra. "Analysis of Slow-Wave Activity and Slow-Wave Oscillations Prior to Somnambulism." Sleep 33, no. 11 (November 2010): 1511–16. http://dx.doi.org/10.1093/sleep/33.11.1511.

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Niethard, Niels, Hong-Viet V. Ngo, Ingrid Ehrlich, and Jan Born. "Cortical circuit activity underlying sleep slow oscillations and spindles." Proceedings of the National Academy of Sciences 115, no. 39 (September 12, 2018): E9220—E9229. http://dx.doi.org/10.1073/pnas.1805517115.

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Slow oscillations and sleep spindles are hallmarks of the EEG during slow-wave sleep (SWS). Both oscillatory events, especially when co-occurring in the constellation of spindles nesting in the slow oscillation upstate, are considered to support memory formation and underlying synaptic plasticity. The regulatory mechanisms of this function at the circuit level are poorly understood. Here, using two-photon imaging in mice, we relate EEG-recorded slow oscillations and spindles to calcium signals recorded from the soma of cortical putative pyramidal-like (Pyr) cells and neighboring parvalbumin-positive interneurons (PV-Ins) or somatostatin-positive interneurons (SOM-Ins). Pyr calcium activity was increased more than threefold when spindles co-occurred with slow oscillation upstates compared with slow oscillations or spindles occurring in isolation. Independent of whether or not a spindle was nested in the slow oscillation upstate, the slow oscillation downstate was preceded by enhanced calcium signal in SOM-Ins that vanished during the upstate, whereas spindles were associated with strongly increased PV-In calcium activity. Additional wide-field calcium imaging of Pyr cells confirmed the enhanced calcium activity and its widespread topography associated with spindles nested in slow oscillation upstates. In conclusion, when spindles are nested in slow oscillation upstates, maximum Pyr activity appears to concur with strong perisomatic inhibition of Pyr cells via PV-Ins and low dendritic inhibition via SOM-Ins (i.e., conditions that might optimize synaptic plasticity within local cortical circuits).

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Kaltiainen, Hanna-Leena, Liisa M. Helle, Hanna M. L. Renvall, and Nina H. Forss. "Slow-Wave Oscillations in Awake Healthy Subjects." Journal of Clinical Neurophysiology 33, no. 4 (August 2016): 367–72. http://dx.doi.org/10.1097/wnp.0000000000000251.

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Wei, Yina, Giri P. Krishnan, and Maxim Bazhenov. "Neuronal plasticity during sleep slow wave oscillations." BMC Neuroscience 15, Suppl 1 (2014): P216. http://dx.doi.org/10.1186/1471-2202-15-s1-p216.

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Valderrama, Mario, Benoît Crépon, Vicente Botella-Soler, Jacques Martinerie, Dominique Hasboun, Catalina Alvarado-Rojas, Michel Baulac, Claude Adam, Vincent Navarro, and Michel Le Van Quyen. "Human Gamma Oscillations during Slow Wave Sleep." PLoS ONE 7, no. 4 (April 4, 2012): e33477. http://dx.doi.org/10.1371/journal.pone.0033477.

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Amini, B., J. W. Clark, and C. C. Canavier. "Calcium Dynamics Underlying Pacemaker-Like and Burst Firing Oscillations in Midbrain Dopaminergic Neurons: A Computational Study." Journal of Neurophysiology 82, no. 5 (November 1, 1999): 2249–61. http://dx.doi.org/10.1152/jn.1999.82.5.2249.

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A mathematical model of midbrain dopamine neurons has been developed to understand the mechanisms underlying two types of calcium-dependent firing patterns that these cells exhibit in vitro. The first is the regular, pacemaker-like firing exhibited in a slice preparation, and the second is a burst firing pattern sometimes exhibited in the presence of apamin. Because both types of oscillations are blocked by nifedipine, we have focused on the slow calcium dynamics underlying these firing modes. The underlying oscillations in membrane potential are best observed when action potentials are blocked by the application of TTX. This converts the regular single-spike firing mode to a slow oscillatory potential (SOP) and apamin-induced bursting to a slow square-wave oscillation. We hypothesize that the SOP results from the interplay between the L-type calcium current (ICa,L) and the apamin-sensitive calcium-activated potassium current ( I K,Ca,SK). We further hypothesize that the square-wave oscillation results from the alternating voltage activation and calcium inactivation of I Ca,L. Our model consists of two components: a Hodgkin-Huxley-type membrane model and a fluid compartment model. A material balance on Ca2+ is provided in the cytosolic fluid compartment, whereas calcium concentration is considered constant in the extracellular compartment. Model parameters were determined using both voltage-clamp and calcium-imaging data from the literature. In addition to modeling the SOP and square-wave oscillations in dopaminergic neurons, the model provides reasonable mimicry of the experimentally observed response of SOPs to TEA application and elongation of the plateau duration of the square-wave oscillations in response to calcium chelation.

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Amzica, Florin, and Dag Neckelmann. "Membrane Capacitance of Cortical Neurons and Glia During Sleep Oscillations and Spike-Wave Seizures." Journal of Neurophysiology 82, no. 5 (November 1, 1999): 2731–46. http://dx.doi.org/10.1152/jn.1999.82.5.2731.

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Dual intracellular recordings in vivo were used to disclose relationships between cortical neurons and glia during spontaneous slow (<1 Hz) sleep oscillations and spike-wave (SW) seizures in cat. Glial cells displayed a slow membrane potential oscillation (<1 Hz), in close synchrony with cortical neurons. In glia, each cycle of this oscillation was made of a round depolarizing potential of 1.5–3 mV. The depolarizing slope corresponded to a steady depolarization and sustained synaptic activity in neurons (duration, 0.5–0.8 s). The repolarization of the glial membrane (duration, 0.5–0.8 s) coincided with neuronal hyperpolarization, associated with disfacilitation, and suppressed synaptic activity in cortical networks. SW seizures in glial cells displayed phasic events, synchronized with neuronal paroxysmal potentials, superimposed on a plateau of depolarization, that lasted for the duration of the seizure. Measurements of the neuronal membrane capacitance during slow oscillating patterns showed small fluctuations around the resting values in relation to the phases of the slow oscillation. In contrast, the glial capacitance displayed a small-amplitude oscillation of 1–2 Hz, independent of phasic sleep and seizure activity. Additionally, in both cell types, SW seizures were associated with a modulatory, slower oscillation (≈0.2 Hz) and a persistent increase of capacitance, developing in parallel with the progression of the seizure. These capacitance variations were dependent on the severity of the seizure and the distance between the presumed seizure focus and the recording site. We suggest that the capacitance variations may reflect changes in the membrane surface area (swelling) and/or of the interglial communication via gap junctions, which may affect the synchronization and propagation of paroxysmal activities.

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Dalal, S. S., C. M. Hamame, J. B. Eichenlaub, and K. Jerbi. "Intrinsic Coupling between Gamma Oscillations, Neuronal Discharges, and Slow Cortical Oscillations during Human Slow-Wave Sleep." Journal of Neuroscience 30, no. 43 (October 27, 2010): 14285–87. http://dx.doi.org/10.1523/jneurosci.4275-10.2010.

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DESTEXHE, A., and T. J. SEJNOWSKI. "Interactions Between Membrane Conductances Underlying Thalamocortical Slow-Wave Oscillations." Physiological Reviews 83, no. 4 (October 2003): 1401–53. http://dx.doi.org/10.1152/physrev.00012.2003.

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Destexhe, A., and T. J. Sejnowski. Interactions Between Membrane Conductances Underlying Thalamocortical Slow-Wave Oscillations. Physiol Rev 83: 1401-1453, 2003; 10.1152/physrev.00012.2003.—Neurons of the central nervous system display a broad spectrum of intrinsic electrophysiological properties that are absent in the traditional “integrate-and-fire” model. A network of neurons with these properties interacting through synaptic receptors with many time scales can produce complex patterns of activity that cannot be intuitively predicted. Computational methods, tightly linked to experimental data, provide insights into the dynamics of neural networks. We review this approach for the case of bursting neurons of the thalamus, with a focus on thalamic and thalamocortical slow-wave oscillations. At the single-cell level, intrinsic bursting or oscillations can be explained by interactions between calcium- and voltage-dependent channels. At the network level, the genesis of oscillations, their initiation, propagation, termination, and large-scale synchrony can be explained by interactions between neurons with a variety of intrinsic cellular properties through different types of synaptic receptors. These interactions can be altered by neuromodulators, which can dramatically shift the large-scale behavior of the network, and can also be disrupted in many ways, resulting in pathological patterns of activity, such as seizures. We suggest a coherent framework that accounts for a large body of experimental data at the ion-channel, single-cell, and network levels. This framework suggests physiological roles for the highly synchronized oscillations of slow-wave sleep.

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Amzica, F. "Cortical slow sleep oscillations developing into spike-wave seizures." Electroencephalography and Clinical Neurophysiology 103, no. 1 (July 1997): 62. http://dx.doi.org/10.1016/s0013-4694(97)88183-0.

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Minamisawa, Genki, Naoya Takahashi, Norio Matsuki, and Yuji Ikegaya. "Laterality of neocortical slow-wave oscillations in anesthetized mice." Neuroscience Research 64, no. 2 (June 2009): 240–42. http://dx.doi.org/10.1016/j.neures.2009.02.006.

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Zhang, Hao, Shih-Chieh Lin, and Miguel A. L. Nicolelis. "A distinctive subpopulation of medial septal slow-firing neurons promote hippocampal activation and theta oscillations." Journal of Neurophysiology 106, no. 5 (November 2011): 2749–63. http://dx.doi.org/10.1152/jn.00267.2011.

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The medial septum-vertical limb of the diagonal band of Broca (MSvDB) is important for normal hippocampal functions and theta oscillations. Although many previous studies have focused on understanding how MSVDB neurons fire rhythmic bursts to pace hippocampal theta oscillations, a significant portion of MSVDB neurons are slow-firing and thus do not pace theta oscillations. The function of these MSVDB neurons, especially their role in modulating hippocampal activity, remains unknown. We recorded MSVDB neuronal ensembles in behaving rats, and identified a distinct physiologically homogeneous subpopulation of slow-firing neurons (overall firing <4 Hz) that shared three features: 1) much higher firing rate during rapid eye movement sleep than during slow-wave (SW) sleep; 2) temporary activation associated with transient arousals during SW sleep; 3) brief responses (latency 15∼30 ms) to auditory stimuli. Analysis of the fine temporal relationship of their spiking and theta oscillations showed that unlike the theta-pacing neurons, the firing of these “pro-arousal” neurons follows theta oscillations. However, their activity precedes short-term increases in hippocampal oscillation power in the theta and gamma range lasting for a few seconds. Together, these results suggest that these pro-arousal slow-firing MSvDB neurons may function collectively to promote hippocampal activation.

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Luna-Cardozo, M., G. Verth, and R. Erdélyi. "Magneto-seismology of solar atmospheric loops by means of longitudinal oscillations." Proceedings of the International Astronomical Union 7, S286 (October 2011): 437–40. http://dx.doi.org/10.1017/s1743921312005224.

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AbstractThere is increasingly strong observational evidence that slow magnetoacoustic modes arise in the solar atmosphere. Solar magneto-seismology is a novel tool to derive otherwise directly un-measurable properties of the solar atmosphere when magnetohydrodynamic (MHD) wave theory is compared to wave observations. Here, MHD wave theory is further developed illustrating how information about the magnetic and density structure along coronal loops can be determined by measuring the frequencies of the slow MHD oscillations. The application to observations of slow magnetoacoustic waves in coronal loops is discussed.

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Castelnovo, Anna, Matteo Zago, Cecilia Casetta, Caroline Zangani, Francesco Donati, Mariapaola Canevini, Brady A. Riedner, et al. "Slow wave oscillations in Schizophrenia First-Degree Relatives: A confirmatory analysis and feasibility study on slow wave traveling." Schizophrenia Research 221 (July 2020): 37–43. http://dx.doi.org/10.1016/j.schres.2020.03.025.

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Чижонков, Е. В., and А. А. Фролов. "Numerical simulation of a slow extraordinary wave in magnetoactive plasma." Numerical Methods and Programming (Vychislitel'nye Metody i Programmirovanie), no. 4 (October 8, 2020): 420–39. http://dx.doi.org/10.26089/nummet.v21r434.

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Численно и аналитически исследовано влияние внешнего магнитного поля на плоские нерелятивистские нелинейные плазменные колебания. Для инициализации медленной необыкновенной волны в магнитоактивной плазме предложен способ построения недостающих начальных условий на основе решения линейной задачи методом Фурье. С целью численного моделирования нелинейной волны построена схема метода конечных разностей второго порядка точности типа МакКормака на основе эйлеровых переменных. Показано, что при учете внешнего магнитного поля ленгмюровские колебания трансформируются в медленную необыкновенную волну, энергия которой вибрирует при перемещении от начала координат. При этом скорость волны увеличивается с ростом внешнего постоянного поля, что способствует выносу энергии из первоначальной области локализации колебаний. The effect of an external magnetic field on plane non-relativistic nonlinear plasma oscillations is studied numerically and analytically. A method for the initialization a slow extraordinary wave in a magnetoactive plasma is proposed for constructing the missing initial conditions based on solving a linear problem using the Fourier method. For the purpose of numerical simulation of a nonlinear wave, a scheme of the second-order accuracy finite difference method of the MacCormack type based on Euler variables is constructed. It is shown that, when the external magnetic field is taken into account, the Langmuir oscillations are transformed into a slow extraordinary wave whose energy vibrates when moving from the origin. In this case, the wave velocity increases with the growth of the external constant field, which contributes to the removal of energy from the initial region of localization of oscillations.

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He, M., M. J. Prerau, and T. S. Dimitrov. "0437 Characterizing the Impact of EEG Referencing on Sleep Spindle and Slow Oscillation Analyses." Sleep 43, Supplement_1 (April 2020): A167—A168. http://dx.doi.org/10.1093/sleep/zsaa056.434.

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Abstract Introduction The impact of EEG referencing on sleep oscillations, such as spindles and slow oscillations, is largely overlooked across studies. While it is recognized that a topographic head plot of EEG activity does not reflect the true location of the underlying cortical activity, spatial distributions, as well as spectral properties and morphology of EEG oscillations can change dramatically as a function of referencing scheme. It is therefore vital to understand the impact of referencing when drawing inferences about the nature of EEG sleep oscillations. In this study, we use MRI structural data to construct subject-specific forward models of EEG signals. Using these models, we can simulate cortical activity and observe its true representation on the scalp. In particular, we simulate spindles and slow wave oscillations and examine how referencing affects topography, spectral power, and phase of oscillations. Methods High-density EEG (Brain Vision, 64-channel) polysomnography was performed on 9 healthy young subjects. 3T structural MRI scans were acquired and forward models were built in MNE-Python using 3-shell Boundary Element Models (BEM) based on individual anatomical details processed with Freesurfer. Simulations of various sleep spindle and slow oscillation dynamics were projected to the sensor space. Different referencing schemes (common average, Laplacian, linked-mastoid) were then applied to the experimental and simulated data and analyzed for effects on time-frequency characteristics of sleep oscillations. Results Analyses of experimental data showed distinct reference-based differences in topographical distribution of spectral power and phase of oscillations. Simulated data revealed many scenarios in which the spatial distribution of activity the EEG sensor space poorly represented the true location of the underlying source activity. Moreover, there were alterations to the spatial spread and envelope form of sleep spindle events under different referencing schemes despite from identical source activities. Conclusion This study shows that spindle and slow oscillation activity is highly variable across referencing schemes and that EEG topographical plots on the scalp may poorly represent cortical activity locations. It is thus vital to consider the choice of referencing when quantifying characteristics of sleep EEG oscillations. Support This work was supported by R01 NS-096177.

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Grenier, François, Igor Timofeev, and Mircea Steriade. "Focal Synchronization of Ripples (80–200 Hz) in Neocortex and Their Neuronal Correlates." Journal of Neurophysiology 86, no. 4 (October 1, 2001): 1884–98. http://dx.doi.org/10.1152/jn.2001.86.4.1884.

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Field potentials from different neocortical areas and intracellular recordings from areas 5 and 7 in acutely prepared cats under ketamine-xylazine anesthesia and during natural states of vigilance in chronic experiments, revealed the presence of fast oscillations (80–200 Hz), termed ripples. During anesthesia and slow-wave sleep, these oscillations were selectively related to the depth-negative (depolarizing) component of the field slow oscillation (0.5–1 Hz) and could be synchronized over ∼10 mm. The dependence of ripples on neuronal depolarization was also shown by their increased amplitude in field potentials in parallel with progressively more depolarized values of the membrane potential of neurons. The origin of ripples was intracortical as they were also detected in small isolated slabs from the suprasylvian gyrus. Of all types of electrophysiologically identified neocortical neurons, fast-rhythmic-bursting and fast-spiking cells displayed the highest firing rates during ripples. Although linked with neuronal excitation, ripples also comprised an important inhibitory component. Indeed, when regular-spiking neurons were recorded with chloride-filled pipettes, their firing rates increased and their phase relation with ripples was modified. Thus besides excitatory connections, inhibitory processes probably play a major role in the generation of ripples. During natural states of vigilance, ripples were generally more prominent during the depolarizing component of the slow oscillation in slow-wave sleep than during the states of waking and rapid-eye movement (REM) sleep. The mechanisms of generation and synchronization, and the possible functions of neocortical ripples in plasticity processes are discussed.

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Lites, Bruce W., Robert J. Rutten, and Wolfgang Kalkofen. "Oscillations of the Magnetic Network." International Astronomical Union Colloquium 141 (1993): 530–33. http://dx.doi.org/10.1017/s0252921100029778.

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AbstractWe present high-quality power spectra of oscillations in the quiet solar chromosphere measured from the Ca II H line. They show unambiguously that the network does not participate in chromospheric three-minute oscillations, but that instead it oscillates in slow wave motions which are neither present in the surrounding non-magnetic chromosphere, nor in the underlying photosphere.

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Le Van Quyen, Michel, Lyle E. Muller, Bartosz Telenczuk, Eric Halgren, Sydney Cash, Nicholas G. Hatsopoulos, Nima Dehghani, and Alain Destexhe. "High-frequency oscillations in human and monkey neocortex during the wake–sleep cycle." Proceedings of the National Academy of Sciences 113, no. 33 (August 1, 2016): 9363–68. http://dx.doi.org/10.1073/pnas.1523583113.

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Beta (β)- and gamma (γ)-oscillations are present in different cortical areas and are thought to be inhibition-driven, but it is not known if these properties also apply to γ-oscillations in humans. Here, we analyze such oscillations in high-density microelectrode array recordings in human and monkey during the wake–sleep cycle. In these recordings, units were classified as excitatory and inhibitory cells. We find that γ-oscillations in human and β-oscillations in monkey are characterized by a strong implication of inhibitory neurons, both in terms of their firing rate and their phasic firing with the oscillation cycle. The β- and γ-waves systematically propagate across the array, with similar velocities, during both wake and sleep. However, only in slow-wave sleep (SWS) β- and γ-oscillations are associated with highly coherent and functional interactions across several millimeters of the neocortex. This interaction is specifically pronounced between inhibitory cells. These results suggest that inhibitory cells are dominantly involved in the genesis of β- and γ-oscillations, as well as in the organization of their large-scale coherence in the awake and sleeping brain. The highest oscillation coherence found during SWS suggests that fast oscillations implement a highly coherent reactivation of wake patterns that may support memory consolidation during SWS.

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Amzica, Florin, and Mircea Steriade. "Spontaneous and Artificial Activation of Neocortical Seizures." Journal of Neurophysiology 82, no. 6 (December 1, 1999): 3123–38. http://dx.doi.org/10.1152/jn.1999.82.6.3123.

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The aim of this study is to disclose the mechanisms underlying the recruitment of neocortical networks during slow-wave sleep oscillations evolving into spike-wave (SW) seizures. 1) We investigated the activation of SW seizures in a seizure-prone neocortex by means of electrical stimuli applied within the frequency range of spontaneous sleep oscillations. Stimuli were grouped in bursts of 10 Hz, similar to sleep spindles, and repeated every 2 s, to reproduce their rhythmic recurrence imposed by the slow (<1 Hz) sleep oscillation. Either cortical or thalamic stimuli, which were applied while the cortex displayed sleeplike activity, gradually induced paroxysmal responses in intracellularly recorded neocortical neurons, which were virtually identical to those of spontaneous seizures and consisted of a progressive buildup of paroxysmal depolarizing shifts (PDSs). 2) The ability of cortical networks to follow stimuli was tested at various stimulation frequencies (1–3 Hz) and quantified by calculating the entropy of the ensuing oscillation. Rhythmic PDSs were optimally induced, and the lowest entropy was generated, at a stimulation frequency around 1.5 Hz. Fast runs at 10–15 Hz, which often override PDSs, thus contributing to the polyspike-wave pattern of seizures, were induced by cortical stimuli, but were disturbed by thalamic stimuli. Spontaneous seizures generally evolved toward an accelerated discharge of PDSs. It is suggested that these accelerating trends during SW seizures act as protective mechanisms by provoking the uncoupling of cortical networks and eventually arresting the seizure.

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Zhao, X., J. W. Kim, and P. A. Robinson. "Slow-wave oscillations in a corticothalamic model of sleep and wake." Journal of Theoretical Biology 370 (April 2015): 93–102. http://dx.doi.org/10.1016/j.jtbi.2015.01.028.

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Luthringer, R., G. Brandenberger, N. Schaltenbrand, G. Muller, K. Spiegel, J. P. Macher, A. Muzet, and M. Follénius. "Slow wave electroencephalic activity parallels renin oscillations during sleep in humans." Electroencephalography and Clinical Neurophysiology 95, no. 5 (November 1995): 318–22. http://dx.doi.org/10.1016/0013-4694(94)00119-6.

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Tucker, Don M., Allison C. Waters, and Mark D. Holmes. "Transition from cortical slow oscillations of sleep to spike-wave seizures." Clinical Neurophysiology 120, no. 12 (December 2009): 2055–62. http://dx.doi.org/10.1016/j.clinph.2009.07.047.

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Cheng, Sen, and Markus Werning. "Composition and replay of mnemonic sequences: The contributions of REM and slow-wave sleep to episodic memory." Behavioral and Brain Sciences 36, no. 6 (November 21, 2013): 610–11. http://dx.doi.org/10.1017/s0140525x13001234.

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AbstractWe propose that rapid eye movement (REM) and slow-wave sleep contribute differently to the formation of episodic memories. REM sleep is important for building up invariant object representations that eventually recur to gamma-band oscillations in the neocortex. In contrast, slow-wave sleep is more directly involved in the consolidation of episodic memories through replay of sequential neural activity in hippocampal place cells.

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Perl, Ofer, Anat Arzi, Lee Sela, Lavi Secundo, Yael Holtzman, Perry Samnon, Arie Oksenberg, Noam Sobel, and Ilana S. Hairston. "Odors enhance slow-wave activity in non-rapid eye movement sleep." Journal of Neurophysiology 115, no. 5 (May 1, 2016): 2294–302. http://dx.doi.org/10.1152/jn.01001.2015.

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Most forms of suprathreshold sensory stimulation perturb sleep. In contrast, presentation of pure olfactory or mild trigeminal odorants does not lead to behavioral or physiological arousal. In fact, some odors promote objective and subjective measures of sleep quality in humans and rodents. The brain mechanisms underlying these sleep-protective properties of olfaction remain unclear. Slow oscillations in the electroencephalogram (EEG) are a marker of deep sleep, and K complexes (KCs) are an EEG marker of cortical response to sensory interference. We therefore hypothesized that odorants presented during sleep will increase power in slow EEG oscillations. Moreover, given that odorants do not drive sleep interruption, we hypothesized that unlike other sensory stimuli odorants would not drive KCs. To test these hypotheses we used polysomnography to measure sleep in 34 healthy subjects (19 women, 15 men; mean age 26.5 ± 2.5 yr) who were repeatedly presented with odor stimuli via a computer-controlled air-dilution olfactometer over the course of a single night. Each participant was exposed to one of four odorants, lavender oil ( n = 13), vetiver oil ( n = 5), vanillin ( n = 12), or ammonium sulfide ( n = 4), for durations of 5, 10, and 20 s every 9–15 min. Consistent with our hypotheses, we found that odor presentation during sleep enhanced the power of delta (0.5–4 Hz) and slow spindle (9–12 Hz) frequencies during non-rapid eye movement sleep. The increase was proportionate to odor duration. In addition, odor presentation did not modulate the occurrence of KCs. These findings imply a sleep-promoting olfactory mechanism that may deepen sleep through driving increased slow-frequency oscillations.

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Kolotkov, D. Y., V. M. Nakariakov, and D. I. Zavershinskii. "Damping of slow magnetoacoustic oscillations by the misbalance between heating and cooling processes in the solar corona." Astronomy & Astrophysics 628 (August 2019): A133. http://dx.doi.org/10.1051/0004-6361/201936072.

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Context. Rapidly decaying slow magnetoacoustic waves are regularly observed in the solar coronal structures, offering a promising tool for a seismological diagnostics of the coronal plasma, including its thermodynamical properties. Aims. The effect of damping of standing slow magnetoacoustic oscillations in the solar coronal loops is investigated accounting for field-aligned thermal conductivity and a wave-induced misbalance between radiative cooling and some unspecified heating rates. Methods. The non-adiabatic terms were allowed to be arbitrarily large, corresponding to the observed values. The thermal conductivity was taken in its classical form, and a power-law dependence of the heating function on the density and temperature was assumed. The analysis was conducted in the linear regime and in the infinite magnetic field approximation. Results. The wave dynamics is found to be highly sensitive to the characteristic timescales of the thermal misbalance. Depending on certain values of the misbalance, timescales three regimes of the wave evolution were identified, namely the regime of a suppressed damping, enhanced damping in which the damping rate drops down to observational values, and acoustic over-stability. The specific regime is determined by the dependences of the radiative cooling and heating functions on thermodynamical parameters of the plasma in the vicinity of the perturbed thermal equilibrium. Conclusions. The comparison of the observed and theoretically derived decay times and oscillation periods allows us to constrain the coronal heating function. For typical coronal parameters, the observed properties of standing slow magnetoacoustic oscillations could be readily reproduced with a reasonable choice of the heating function.

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Torres, Felipe A., Patricio Orio, and María-José Escobar. "Selection of stimulus parameters for enhancing slow wave sleep events with a neural-field theory thalamocortical model." PLOS Computational Biology 17, no. 7 (July 30, 2021): e1008758. http://dx.doi.org/10.1371/journal.pcbi.1008758.

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Slow-wave sleep cortical brain activity, conformed by slow-oscillations and sleep spindles, plays a key role in memory consolidation. The increase of the power of the slow-wave events, obtained by auditory sensory stimulation, positively correlates with memory consolidation performance. However, little is known about the experimental protocol maximizing this effect, which could be induced by the power of slow-oscillation, the number of sleep spindles, or the timing of both events’ co-occurrence. Using a mean-field model of thalamocortical activity, we studied the effect of several stimulation protocols, varying the pulse shape, duration, amplitude, and frequency, as well as a target-phase using a closed-loop approach. We evaluated the effect of these parameters on slow-oscillations (SO) and sleep-spindles (SP), considering: (i) the power at the frequency bands of interest, (ii) the number of SO and SP, (iii) co-occurrences between SO and SP, and (iv) synchronization of SP with the up-peak of the SO. The first three targets are maximized using a decreasing ramp pulse with a pulse duration of 50 ms. Also, we observed a reduction in the number of SO when increasing the stimulus energy by rising its amplitude. To assess the target-phase parameter, we applied closed-loop stimulation at 0°, 45°, and 90° of the phase of the narrow-band filtered ongoing activity, at 0.85 Hz as central frequency. The 0° stimulation produces better results in the power and number of SO and SP than the rhythmic or random stimulation. On the other hand, stimulating at 45° or 90° change the timing distribution of spindles centers but with fewer co-occurrences than rhythmic and 0° phase. Finally, we propose the application of closed-loop stimulation at the rising zero-cross point using pulses with a decreasing ramp shape and 50 ms of duration for future experimental work.

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Canavier, C. C., J. W. Clark, and J. H. Byrne. "Simulation of the bursting activity of neuron R15 in Aplysia: role of ionic currents, calcium balance, and modulatory transmitters." Journal of Neurophysiology 66, no. 6 (December 1, 1991): 2107–24. http://dx.doi.org/10.1152/jn.1991.66.6.2107.

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1. An equivalent circuit model of the R15 bursting neuron in Aplysia has been combined with a fluid compartment model, resulting in a model that incorporates descriptions of most of the membrane ion channels that are known to exist in the somata of R15, as well as providing a Ca2+ balance on the cell. 2. A voltage-activated, calcium-inactivated Ca2+ current (denoted the slow inward current ISI) was sufficient to produce bursting activity without invoking any other calcium-dependent currents (such as a nonspecific cation current, INS, or a calcium-activated K+ current, IK,Ca). Furthermore, many characteristics of a typical R15 burst could be simulated, such as a parabolic variation in interspike interval, the depolarizing afterpotential (DAP), and the progressive decrease in the undershoots of spikes during a burst. 3. The dynamic activity of R15 was analyzed by separately characterizing two different temporal domains; the fast dynamics associated with action potentials and the slow dynamics associated with low-amplitude oscillations lasting tens of seconds ("slow waves"). The slow dynamics were isolated by setting the Na+ conductance (gNa) to zero and then studied by the use of a system of equations reduced to two variables: intracellular concentration of Ca2+ and membrane potential. The fixed point of the system was located at the intersection of the nullclines for these two variables. A stability analysis of the fixed point was then used to determine whether a given set of parameters would produce slow-wave activity. 4. If the reduced model predicted slow-wave oscillations for a given set of parameters with gNa set to zero, then bursting activity was observed for the same set of parameters in the full model with gNa reset to its control value. However, for certain sets of parameters with gNa at its usual value, the full model exhibited bursting activity because of a slow oscillation produced by the activation of INS by action potentials. This oscillation resulted from an interaction between the fast and slow dynamics that the reduced model alone could not predict and was not observed when gNa was subsequently set to zero. If gNS was also set to zero, this discrepancy disappeared.(ABSTRACT TRUNCATED AT 400 WORDS)

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Hansen, Allan Kjeldsen, Steen Nedergaard, and Mogens Andreasen. "Intrinsic Ca2+-dependent theta oscillations in apical dendrites of hippocampal CA1 pyramidal cells in vitro." Journal of Neurophysiology 112, no. 3 (August 1, 2014): 631–43. http://dx.doi.org/10.1152/jn.00753.2013.

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Behavior-associated theta-frequency oscillation in the hippocampal network involves a patterned activation of place cells in the CA1, which can be accounted for by a somatic-dendritic interference model predicting the existence of an intrinsic dendritic oscillator. Here we describe an intrinsic oscillatory mechanism in apical dendrites of in vitro CA1 pyramidal cells, which is induced by suprathreshold depolarization and consists of rhythmic firing of slow spikes in the theta-frequency band. The incidence of slow spiking (29%) increased to 78% and 100% in the presence of the β-adrenergic agonist isoproterenol (2 μM) or 4-aminopyridine (2 mM), respectively. Prior depolarization facilitated the induction of slow spiking. Applied electrical field polarization revealed a distal dendritic origin of slow spikes. The oscillations were largely insensitive to tetrodotoxin, but blocked by nimodipine (10 μM), indicating that they depend on activation of L-type Ca2+ channels. Antagonists of T-, R-, N-, and P/Q-type Ca2+ channels had no detectable effect. The slow spike dimension and frequency was sensitive to 4-aminopyridine (0.1–2 mM) and TEA (10 mM), suggesting the contribution from voltage-dependent K+ channels to the oscillation mechanism. α-Dendrotoxin (10 μM), stromatoxin (2 μM), iberiotoxin (0.2 μM), apamin (0.5 μM), linorpidine (30 μM), and ZD7288 (20 μM) were without effect. Oscillations induced by sine-wave current injection or theta-burst synaptic stimulation were voltage-dependently attenuated by nimodipine, indicating an amplifying function of L-type Ca2+ channels on imposed signals. These results show that the apical dendrites have intrinsic oscillatory properties capable of generating rhythmic voltage fluctuations in the theta-frequency band.

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Ward, S. M., R. G. Keller, and K. M. Sanders. "Structure and organization of electrical activity of canine distal colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 5 (May 1, 1991): G724—G735. http://dx.doi.org/10.1152/ajpgi.1991.260.5.g724.

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The morphology and electrophysiology of the canine distal colon were studied to compare this region with the proximal colon. Many morphological characteristics were similar including the presence of interstitial cells at the submucosal surface of the circular layer. Muscle cells near the submucosal surface had resting membrane potentials (RMPs) of -79 +/- 1 mV, and slow waves were generated in this region. Slow waves had similar waveform characteristics to those of the proximal colon, but rapid oscillations were superimposed on slow waves of some preparations. RMPs and slow waves decreased with distance from the submucosal surface. The latter were not resolvable in the myenteric half of the circular layer. Cells at the myenteric border had RMPs of -49.5 +/- 2 mV and a higher frequency oscillation of 16 min-1. Acetylcholine increased slow-wave amplitude and duration and caused fast oscillations on the plateau phase of slow waves. Isolated circular myocytes were studied with the patch-clamp technique. Cells from the submucosal border displayed voltage-dependent inward and outward currents. With outward currents blocked, the inward current was composed of two components. Nifedipine (10(-6) M) blocked a portion of the inward current but left a substantial transient component. The effect of nifedipine correlated with its effects on tissues, suggesting that two components of Ca2+ current participate in slow waves. These studies describe numerous similarities in the structure and activity of the proximal and distal portions of the colon but also show some potentially important differences between these regions.

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Favero, Morgana, Gladis Varghese, and Manuel A. Castro-Alamancos. "The state of somatosensory cortex during neuromodulation." Journal of Neurophysiology 108, no. 4 (August 15, 2012): 1010–24. http://dx.doi.org/10.1152/jn.00256.2012.

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During behavioral quiescence, such as slow-wave sleep and anesthesia, the neocortex is in a deactivated state characterized by the presence of slow oscillations. During arousal, slow oscillations are absent and the neocortex is in an activated state that greatly impacts information processing. Neuromodulators acting in neocortex are believed to mediate these state changes, but the mechanisms are poorly understood. We investigated the actions of noradrenergic and cholinergic activation on slow oscillations, cellular excitability, and synaptic inputs in thalamocortical slices of somatosensory cortex. The results show that neuromodulation abolishes slow oscillations, dampens the excitability of principal cells, and rebalances excitatory and inhibitory synaptic inputs in thalamocortical-recipient layers IV–III. Sensory cortex is much more selective about the inputs that can drive it. The source of neuromodulation is critically important in determining this selectivity. Cholinergic activation suppresses the excitatory and inhibitory conductances driven by thalamocortical and intracortical inputs. Noradrenergic activation suppresses the excitatory conductance driven by intracortical inputs but not by thalamocortical inputs and enhances the inhibitory conductance driven by thalamocortical inputs but not by intracortical inputs. Thus noradrenergic activation emphasizes thalamocortical (sensory) inputs relative to intracortical inputs, while cholinergic activation suppresses both.

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35

Manabe, Hiroyuki, and Kensaku Mori. "Sniff rhythm-paced fast and slow gamma-oscillations in the olfactory bulb: relation to tufted and mitral cells and behavioral states." Journal of Neurophysiology 110, no. 7 (October 1, 2013): 1593–99. http://dx.doi.org/10.1152/jn.00379.2013.

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Odor signals are conveyed from the olfactory bulb (OB) to the olfactory cortex by two types of projection neurons, tufted cells and mitral cells, which differ in signal timing and firing frequency in response to odor inhalation. Whereas tufted cells respond with early-onset high-frequency burst discharges starting at the middle of the inhalation phase of sniff, mitral cells show odor responses with later-onset lower-frequency burst discharges. Since odor inhalation induces prominent gamma-oscillations of local field potentials (LFPs) in the OB during the transition period from inhalation to exhalation that accompany synchronized spike discharges of tufted cells and mitral cells, we addressed the question of whether the odor-induced gamma-oscillations encompass two distinct gamma-oscillatory sources, tufted cell and mitral cell subsystems, by simultaneously recording the sniff rhythms and LFPs in the OB of freely behaving rats. We observed that individual sniffs induced nested gamma-oscillations with two distinct parts during the inhalation-exhalation transition period: early-onset fast gamma-oscillations followed by later-onset slow gamma-oscillations. These results suggest that tufted cells carry odor signals with early-onset fast gamma-synchronization at the early phase of sniff, whereas mitral cells send them with later-onset slow gamma-synchronization. We also observed that each sniff typically induced both fast and slow gamma-oscillations during awake, whereas respiration during slow-wave sleep and rapid-eye-movement sleep failed to induce these oscillations. These results suggest that behavioral states regulate the generation of sniff rhythm-paced fast and slow gamma-oscillations in the OB.

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36

Longtin, André, and Karin Hinzer. "Encoding with Bursting, Subthreshold Oscillations, and Noise in Mammalian Cold Receptors." Neural Computation 8, no. 2 (February 15, 1996): 215–55. http://dx.doi.org/10.1162/neco.1996.8.2.215.

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Mammalian cold thermoreceptors encode steady-state temperatures into characteristic temporal patterns of action potentials. We propose a mechanism for the encoding process. It is based on Plant's ionic model of slow wave bursting, to which stochastic forcing is added. The model reproduces firing patterns from cat lingual cold receptors as the parameters most likely to underlie the thermosensitivity of these receptors varied over a 25°C range. The sequence of firing patterns goes from regular bursting, to simple periodic, to stochastically phase-locked firing or “skipping.” The skipping at higher temperatures is shown to necessitate an interaction between noise and a subthreshold endogenous oscillation in the receptor. The basic period of all patterns is robust to noise. Further, noise extends the range of encodable stimuli. An increase in firing irregularity with temperature also results from the loss of stability accompanying the approach by the slow dynamics of a reverse Hopf bifurcation. The results are not dependent on the precise details of the Plant model, but are generic features of models where an autonomous slow wave arises through a Hopf bifurcation. The model also addresses the variability of the firing patterns across fibers. An alternate model of slow-wave bursting (Chay and Fan 1993) in which skipping can occur without noise is also analyzed here in the context of cold thermoreception. Our study quantifies the possible origins and relative contribution of deterministic and stochastic dynamics to the coding scheme. Implications of our findings for sensory coding are discussed.

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Norimoto, Hiroaki, Kenichi Makino, Mengxuan Gao, Yu Shikano, Kazuki Okamoto, Tomoe Ishikawa, Takuya Sasaki, Hiroyuki Hioki, Shigeyoshi Fujisawa, and Yuji Ikegaya. "Hippocampal ripples down-regulate synapses." Science 359, no. 6383 (February 8, 2018): 1524–27. http://dx.doi.org/10.1126/science.aao0702.

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The specific effects of sleep on synaptic plasticity remain unclear. We report that mouse hippocampal sharp-wave ripple oscillations serve as intrinsic events that trigger long-lasting synaptic depression. Silencing of sharp-wave ripples during slow-wave states prevented the spontaneous down-regulation of net synaptic weights and impaired the learning of new memories. The synaptic down-regulation was dependent on the N-methyl-d-aspartate receptor and selective for a specific input pathway. Thus, our findings are consistent with the role of slow-wave states in refining memory engrams by reducing recent memory-irrelevant neuronal activity and suggest a previously unrecognized function for sharp-wave ripples.

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38

Moskalenko, Yu E., T. I. Kravchenko, G. B. Vainshtein, P. Halvorson, A. Feilding, A. Mandara, A. A. Panov, and V. N. Semernya. "Slow-Wave Oscillations in the Craniosacral Space: A Hemoliquorodynamic Concept of Origination." Neuroscience and Behavioral Physiology 39, no. 4 (April 2, 2009): 377–81. http://dx.doi.org/10.1007/s11055-009-9140-8.

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39

Villalobos, Claudio, Pedro E. Maldonado, and José L. Valdés. "Asynchronous ripple oscillations between left and right hippocampi during slow-wave sleep." PLOS ONE 12, no. 2 (February 3, 2017): e0171304. http://dx.doi.org/10.1371/journal.pone.0171304.

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40

Bazhenov, Maxim, Igor Timofeev, Mircea Steriade, and Terrence J. Sejnowski. "Model of Thalamocortical Slow-Wave Sleep Oscillations and Transitions to Activated States." Journal of Neuroscience 22, no. 19 (October 1, 2002): 8691–704. http://dx.doi.org/10.1523/jneurosci.22-19-08691.2002.

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41

Fucke, Thomas, Dymphie Suchanek, Martin P. Nawrot, Yamina Seamari, Detlef H. Heck, Ad Aertsen, and Clemens Boucsein. "Stereotypical spatiotemporal activity patterns during slow-wave activity in the neocortex." Journal of Neurophysiology 106, no. 6 (December 2011): 3035–44. http://dx.doi.org/10.1152/jn.00811.2010.

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Alternating epochs of activity and silence are a characteristic feature of neocortical networks during certain sleep cycles and deep states of anesthesia. The mechanism and functional role of these slow oscillations (<1 Hz) have not yet been fully characterized. Experimental and theoretical studies show that slow-wave oscillations can be generated autonomously by neocortical tissue but become more regular through a thalamo-cortical feedback loop. Evidence for a functional role of slow-wave activity comes from EEG recordings in humans during sleep, which show that activity travels as stereotypical waves over the entire brain, thought to play a role in memory consolidation. We used an animal model to investigate activity wave propagation on a smaller scale, namely within the rat somatosensory cortex. Signals from multiple extracellular microelectrodes in combination with one intracellular recording in the anesthetized animal in vivo were utilized to monitor the spreading of activity. We found that activity propagation in most animals showed a clear preferred direction, suggesting that it often originated from a similar location in the cortex. In addition, the breakdown of active states followed a similar pattern with slightly weaker direction preference but a clear correlation to the direction of activity spreading, supporting the notion of a wave-like phenomenon similar to that observed after strong sensory stimulation in sensory areas. Taken together, our findings support the idea that activity waves during slow-wave sleep do not occur spontaneously at random locations within the network, as was suggested previously, but follow preferred synaptic pathways on a small spatial scale.

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Carbone, Julia, Carlos Bibián, Patrick Reischl, Jan Born, Cecilia Forcato, and Susanne Diekelmann. "The effect of zolpidem on targeted memory reactivation during sleep." Learning & Memory 28, no. 9 (August 16, 2021): 307–18. http://dx.doi.org/10.1101/lm.052787.120.

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According to the active system consolidation theory, memory consolidation during sleep relies on the reactivation of newly encoded memory representations. This reactivation is orchestrated by the interplay of sleep slow oscillations, spindles, and theta, which are in turn modulated by certain neurotransmitters like GABA to enable long-lasting plastic changes in the memory store. Here we asked whether the GABAergic system and associated changes in sleep oscillations are functionally related to memory reactivation during sleep. We administered the GABAA agonist zolpidem (10 mg) in a double-blind placebo-controlled study. To specifically focus on the effects on memory reactivation during sleep, we experimentally induced such reactivations by targeted memory reactivation (TMR) with learning-associated reminder cues presented during post-learning slow-wave sleep (SWS). Zolpidem significantly enhanced memory performance with TMR during sleep compared with placebo. Zolpidem also increased the coupling of fast spindles and theta to slow oscillations, although overall the power of slow spindles and theta was reduced compared with placebo. In an uncorrected exploratory analysis, memory performance was associated with slow spindle responses to TMR in the zolpidem condition, whereas it was associated with fast spindle responses in placebo. These findings provide tentative first evidence that GABAergic activity may be functionally implicated in memory reactivation processes during sleep, possibly via its effects on slow oscillations, spindles and theta as well as their interplay.

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43

Reznik, G. M. "Wave adjustment: general concept and examples." Journal of Fluid Mechanics 779 (August 18, 2015): 514–43. http://dx.doi.org/10.1017/jfm.2015.391.

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We formulate a general theory of wave adjustment applicable to any physical system (not necessarily a hydrodynamic one), which, being linearized, possesses linear invariants and a complete system of waves harmonically depending on the time $t$. The invariants are determined by the initial conditions and are zero for the waves, which, therefore, do not transport and affect the invariants. The evolution of such a system can be represented naturally as the sum of a stationary component with non-zero invariants and a non-steady wave part with zero invariants. If the linear system is disturbed by a small perturbation (linear or nonlinear), then the state vector of the system is split into slow balanced and fast wave components. Various scenarios of the wave adjustment are demonstrated with fairly simple hydrodynamic models. The simplest scenario, called ‘fast radiation’, takes place when the waves rapidly (their group speed $c_{gr}$ greatly exceeds the slow flow velocity $U$) radiate away from the initial perturbation and do not interact effectively with the slow component. As a result, at large times, after the waves propagate away, the residual flow is slow and described by a balanced model. The scenario is exemplified by the three-dimensional non-rotating barotropic flow with a free surface. A more complicated scenario, called ‘nonlinear trapping’, occurs if oscillations with small group speed $c_{gr}\leqslant U$ are present in the wave spectrum. In this case, after nonlinear wave adjustment, the state vector is a superposition of the slow balanced component and oscillations with small $c_{gr}$ trapped by this component. An example of this situation is the geostrophic adjustment of a three-dimensional rotating barotropic layer with a free surface. In the third scenario, called ‘incomplete splitting’, the wave adjustment is accompanied by non-stationary boundary layers arising near rigid and internal boundaries at large times. The thickness of such a layer tends to zero and cross-gradients of physical parameters in the layer tend to infinity as $t\rightarrow \infty$. The layer is an infinite number of wave modes whose group speed tends to zero as the mode number tends to infinity. In such a system, complete splitting of motion into fast and slow components is impossible even in the linear approximation. The scenario is illustrated by an example of stratified non-rotating flow between two rigid lids. The above scenarios describe, at least, the majority of known cases of wave adjustment.

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Perrault, Rosemarie, Julie Carrier, Alex Desautels, Jacques Montplaisir, and Antonio Zadra. "Slow wave activity and slow oscillations in sleepwalkers and controls: effects of 38 h of sleep deprivation." Journal of Sleep Research 22, no. 4 (February 11, 2013): 430–33. http://dx.doi.org/10.1111/jsr.12041.

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Boswell, R. W., and M. J. Giles. "Period doubling of azimuthal oscillations on a non-neutral magnetized electron column." Journal of Plasma Physics 33, no. 1 (February 1985): 59–69. http://dx.doi.org/10.1017/s0022377800002324.

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We investigate the low-frequency azimuthal oscillations on a non-neutral magnetized electron column of very low density. A perturbation analysis of the slow mode of the rigid rotator equilibrium is developed to illustrate the nature of large-amplitude fundamental-mode oscillations. The results of this theoretical analysis show two important characteristics: firstly, as the perturbation amplitude is increased the wave form ceases to be purely sinusoidal and shows period doubling. Secondly, above a certain threshold, all harmonics of the wave grow and the wave breaks. The results of the former are compared with a simple electron beam experiment and are found to be in good qualitative agreement.

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46

Greenwood, Beverley, Jan D. Huizinga, Edwin Chow, and Wylie J. Dodds. "Relationship between transmural potential difference and smooth muscle slow waves and contractility in the rabbit small intestine in vitro." Canadian Journal of Physiology and Pharmacology 66, no. 9 (September 1, 1988): 1161–65. http://dx.doi.org/10.1139/y88-191.

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The relationship between transmural potential difference (PD) and smooth muscle electrical and mechanical activity was investigated in the rabbit ileum in vitro. Transmural PD was monitored using agar salt bridge electrodes connected via calomel half cells to an electrometer. Force displacement transducers recorded predominantly longitudinal smooth muscle activity. Concurrently, predominantly circular muscle activity was recorded at three sites using intraluminal pressure probes. At the same sites, suction electrodes monitored electrical activity of the smooth muscle. In all experiments, fluctuations in transmural PD were temporally linked to smooth muscle mechanical and electrical activity. The frequency of PD oscillations, electrical slow waves, and cyclic pressure changes were identical within each segment. Adrenaline abolished smooth muscle electrical spiking, all mechanical activity, and transmural fluctuations in PD. However, the slow waves were not abolished, though their frequency was increased. Phentolamine but not propranolol reversed the effects of adrenaline, thus slow wave frequency is influenced by α-adrenergic stimulation in the rabbit ileum. In conclusion, oscillations in transmural PD are unrelated to the ionic processes associated with the slow wave. However, they are in some way linked to smooth muscle contractile activity, possibly via an intrinsic neural mechanism as observed in the guinea pig.

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Harrington, Marcus O., and Scott A. Cairney. "Sounding It Out: Auditory Stimulation and Overnight Memory Processing." Current Sleep Medicine Reports 7, no. 3 (July 16, 2021): 112–19. http://dx.doi.org/10.1007/s40675-021-00207-0.

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Abstract Purpose of Review Auditory stimulation is a technique that can enhance neural oscillations linked to overnight memory consolidation. In this review, we evaluate the impacts of auditory stimulation on the neural oscillations of sleep and associated memory processes in a variety of populations. Recent Findings Cortical EEG recordings of slow-wave sleep (SWS) are characterised by two cardinal oscillations: slow oscillations (SOs) and sleep spindles. Auditory stimulation delivered in SWS enhances SOs and phase-coupled spindle activity in healthy children and adults, children with ADHD, adults with mild cognitive impairment and patients with major depression. Under certain conditions, auditory stimulation bolsters the benefits of SWS for memory consolidation, although further work is required to fully understand the factors affecting stimulation-related memory gains. Recent work has turned to rapid eye movement (REM) sleep, demonstrating that auditory stimulation can be used to manipulate REM sleep theta oscillations. Summary Auditory stimulation enhances oscillations linked to overnight memory processing and shows promise as a technique for enhancing the memory benefits of sleep.

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Olbrich, Eckehard, Thomas Rusterholz, Monique K. LeBourgeois, and Peter Achermann. "Developmental Changes in Sleep Oscillations during Early Childhood." Neural Plasticity 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/6160959.

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Although quantitative analysis of the sleep electroencephalogram (EEG) has uncovered important aspects of brain activity during sleep in adolescents and adults, similar findings from preschool-age children remain scarce. This study utilized our time-frequency method to examine sleep oscillations as characteristic features of human sleep EEG. Data were collected from a longitudinal sample of young children (n=8; 3 males) at ages 2, 3, and 5 years. Following sleep stage scoring, we detected and characterized oscillatory events across age and examined how their features corresponded to spectral changes in the sleep EEG. Results indicated a developmental decrease in the incidence of delta and theta oscillations. Spindle oscillations, however, were almost absent at 2 years but pronounced at 5 years. All oscillatory event changes were stronger during light sleep than slow-wave sleep. Large interindividual differences in sleep oscillations and their characteristics (e.g., “ultrafast” spindle-like oscillations, theta oscillation incidence/frequency) also existed. Changes in delta and spindle oscillations across early childhood may indicate early maturation of the thalamocortical system. Our analytic approach holds promise for revealing novel types of sleep oscillatory events that are specific to periods of rapid normal development across the lifespan and during other times of aberrant changes in neurobehavioral function.

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Raccuglia, Davide, Sheng Huang, Anatoli Ender, M. Marcel Heim, Desiree Laber, Raquel Suárez-Grimalt, Agustin Liotta, Stephan J. Sigrist, Jörg R. P. Geiger, and David Owald. "Network-Specific Synchronization of Electrical Slow-Wave Oscillations Regulates Sleep Drive in Drosophila." Current Biology 29, no. 21 (November 2019): 3611–21. http://dx.doi.org/10.1016/j.cub.2019.08.070.

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Liu, Louis W. C., and Jan D. Huizinga. "Canine colonic circular muscle generates action potentials without the pacemaker component." Canadian Journal of Physiology and Pharmacology 72, no. 1 (January 1, 1994): 70–81. http://dx.doi.org/10.1139/y94-012.

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Abstract:

Two dominant types of action potentials in canine colon are slow wave type action potentials (slow waves) and spike-like action potentials (SLAPs). The slow waves, originating at the submuscular surface where a network of interstitial cells of Cajal (ICCs) is found, possess a pacemaker component. Activation of the pacemaker component is insensitive to voltage changes and L-type calcium channel blockers, and is postulated to involve a metabolic clock sensitive to cyclic AMP. SLAPs are more prominent in the longitudinal muscle. To understand the contribution circular muscle cells make to the generation of these action potentials, a circular muscle preparation (devoid of the submuscular ICC – smooth muscle network, longitudinal muscle, and myenteric plexus) was developed. Circular muscle preparations were spontaneously quiescent, with a resting membrane potential of −62.9 ± 0.6 mV. Ba2+ (0.5 mM) depolarized the cells to −51.8 ± 0.6 mV and induced electrical oscillations with a frequency, duration, amplitude, and rate of rise equal to 6.6 ± 0.4 cpm, 2.2 ± 0.2 s, 19.4 ± 0.9 mV, and 21.8 ± 1.7 mV/s, respectively. In most cases, Ba2+-induced oscillations were preceded by a prepotential of 4.4 ± 0.3 mV, with a rate of rise of 1.1 ± 0.1 mV/s. Ba2+-induced oscillations were abolished by 1 μM D600 as well as by repolarization of 6–12 mV. Addition of 0.1 μM Bay K8644 in the presence of Ba2+ further depolarized circular muscle cells to −42.4 ± 0.8 mV and increased the oscillation frequency to 16.8 ± 1.8 cpm. The electrical oscillations induced in circular muscle preparations by Ba2+ and Bay K8644 were similar to the SLAPs exhibited by the isolated longitudinal muscle layer, indicating that generation of SLAPs is an intrinsic property of smooth muscle cells. Forskolin (1 μM), previously shown to dramatically decrease the frequency but not the amplitude of slow waves in preparations including the submuscular ICC network, decreased the amplitude of the Ba2+-induced oscillations in circular muscle preparations without changing the frequency. These results provide strong evidence for the hypothesis that the submuscular ICC – smooth muscle network is essential for the initiation of the pacemaker component of the colonic slow waves. The mechanism for regulating the frequency of slow waves is different from that responsible for the Ba2+-induced oscillations in circular muscle preparations. Circular muscle cells are shown to be excitable and capable of generating oscillatory activity dominated by L-type calcium channel activity, which is regulated by K+ conductance.Key words: interstitial cells of Cajal, smooth muscle, dog colon, barium chloride, potassium conductance, Bay K8644, pacemaking activity.

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Journal articles on the topic 'Slow-wave oscillations'

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