Neuronal activity in the caudolateral peribrachial pons: relationship to PGO waves and rapid eye movements

1994 ◽  
Vol 71 (1) ◽  
pp. 95-109 ◽  
Author(s):  
S. Datta ◽  
J. A. Hobson
Keyword(s):  
Eye Movements ◽  
Slow Wave ◽  
Rem Sleep ◽  
High Frequency ◽  
Slow Wave Sleep ◽  
Lateral Geniculate Body ◽  
Cellular Level ◽  
Firing Rates ◽  
Rapid Eye Movements ◽  
Pgo Waves

1. The present study was performed to examine the hypothesis that the caudolateral peribrachial area (C-PBL) may be directly involved in shifting the brain from the nonpontogeniculooccipital (non-PGO)-related states of waking (W) and slow-wave sleep (S) to the PGO-related states of slow-wave sleep with PGO waves (SP) and rapid eye movement (REM) sleep. 2. To test this hypothesis at the cellular level, we have recorded a sample of 226 spontaneously discharging units of the C-PBL during natural sleep-waking cycles in unanesthetized head-restrained cats and have correlated the action-potential data with the PGO waves. 3. Of these 226 cells, 67.26% (n = 152) were called PGO state-on units because they increased or began firing 15'5 s before the first PGO wave of SP and maintained their high firing rate throughout SP (31.30 +/- 6.0 Hz, mean +/- SD) and REM sleep (39.46 +/- 6.70 Hz); their firing rates in W (0.45 +/- 0.85) and S (0.70 +/- 1.26) were much lower. Among these PGO state-on neurons, 28.94% (n = 44) discharged high-frequency (> 500 Hz) spike bursts on the background of tonically increased firing rates during the PGO-related states. Contrastingly, 14.16% (n = 32) of the cells (called PGO state-off units) fired tonically during W (11.54 +/- 4.15) and S (9.43 +/- 3.87) but stopped or decreased firing 25–15 s before the first PGO wave of SP; their activity remained suppressed throughout SP (0.19 +/- 0.44) and REM sleep (0.03 +/- 0.17). The remaining 18.58% (n = 42) cells fired (9–10 Hz) tonically but were unrelated to the wake-sleeping cycle. 4. During SP and REM sleep, primary PGO waves were found to appear with equal frequency in each lateral geniculate body (LGB). During REM sleep these primary waves were ipsilateral to the direction of phasic rapid eye movements as previously reported by Nelson et al. (1983). 5. During SP and REM sleep PGO state-on burst cells fired high-frequency bursts on a background of tonic activity in association with each ipsilateral primary LGB PGO wave. The first spike of a burst preceded the beginning of the negative component of the ipsilateral LGB PGO waves by 25 +/- 7.5 ms. On the basis of their sustained firing and the latency of their PGO-related bursting, we call these neurons long-lead PGO-on burst-tonic cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Neostriatal administration of somatostatin: differential effect of small and large doses on behavior and motor control

1977 ◽  
Vol 55 (2) ◽  
pp. 234-242 ◽  
Author(s):  
M. Rezek ◽  
V. Havlicek ◽  
L. Leybin ◽  
C. Pinsky ◽  
E. A. Kroeger ◽  
...  
Keyword(s):  
Motor Control ◽  
Eye Movements ◽  
Slow Wave ◽  
Rem Sleep ◽  
Differential Effect ◽  
Slow Wave Sleep ◽  
Small Doses ◽  
Freely Moving ◽  
Behavioral Excitation ◽  
Higher Doses

The administration of small doses of somatostatin (SRIF) (0.01 and 0.1 μg) into the neostriatal complex of unrestrained, freely moving rats induced general behavioral excitation associated with a variety of stereotyped movements, tremors, and a reduction of rapid eye movements (REM) and deep slow wave sleep (SWS). In contrast, the higher doses of SRIF (1.0 and 10.0 μg) caused movements to be uncoordinated and frequently induced more severe difficulties in motor control such as contralateral hemiplegia-in-extension which restricted or completely prevented the expression of normal behavioral patterns. As a result, the animals appeared drowsy and inhibited. Analysis of the sleep-waking cycle revealed prolonged periods of a shallow SWS while REM sleep and deep SWS were markedly reduced; electroencephalogram recordings revealed periods of dissociation from behavior. The administration of endocrinologically inactive as well as the active analogues of SRIF failed to induce effects comparable with those observed after the administration of the same dose of the native hormone (10.0 μg).

Sleep-Related Electrophysiology and Behavior of Tinamous (Eudromia elegans): Tinamous Do Not Sleep Like Ostriches

2017 ◽  
Vol 89 (4) ◽  
pp. 249-261 ◽  
Author(s):  
Ryan K. Tisdale ◽  
Alexei L. Vyssotski ◽  
John A. Lesku ◽  
Niels C. Rattenborg
Keyword(s):  
Eye Movements ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Muscle Tone ◽  
Slow Waves ◽  
Sleep State ◽  
Rapid Eye Movements ◽  
Electrophysiological Studies ◽  
Taxonomic Groups ◽  
And Behavior

The functions of slow wave sleep (SWS) and rapid eye movement (REM) sleep, distinct sleep substates present in both mammals and birds, remain unresolved. One approach to gaining insight into their function is to trace the evolution of these states through examining sleep in as many taxonomic groups as possible. The mammalian and avian clades are each composed of two extant groups, i.e., the monotremes (echidna and platypus) and therian (marsupial and eutherian [or placental]) mammals, and Palaeognaths (cassowaries, emus, kiwi, ostriches, rheas, and tinamous) and Neognaths (all other birds) among birds. Previous electrophysiological studies of monotremes and ostriches have identified a unique “mixed” sleep state combining features of SWS and REM sleep unlike the well-delineated sleep states observed in all therian mammals and Neognath birds. In the platypus this state is characterized by periods of REM sleep-related myoclonic twitching, relaxed skeletal musculature, and rapid eye movements, occurring in conjunction with SWS-related slow waves in the forebrain electroencephalogram (EEG). A similar mixed state was also observed in ostriches; although in addition to occurring during periods with EEG slow waves, reduced muscle tone and rapid eye movements also occurred in conjunction with EEG activation, a pattern typical of REM sleep in Neognath birds. Collectively, these studies suggested that REM sleep occurring exclusively as an integrated state with forebrain activation might have evolved independently in the therian and Neognath lineages. To test this hypothesis, we examined sleep in the elegant crested tinamou (Eudromia elegans), a small Palaeognath bird that more closely resembles Neognath birds in size and their ability to fly. A 24-h period was scored for sleep state based on electrophysiology and behavior. Unlike ostriches, but like all of the Neognath birds examined, all indicators of REM sleep usually occurred in conjunction with forebrain activation in tinamous. The absence of a mixed REM sleep state in tinamous calls into question the idea that this state is primitive among Palaeognath birds and therefore birds in general.

Human cerebral potentials associated with REM sleep rapid eye movements: links to PGO waves and waking potentials

1983 ◽  
Vol 274 (2) ◽  
pp. 359-364 ◽  
Author(s):  
Robert W. McCarley ◽  
John W. Winkelman ◽  
Frank H. Duffy
Keyword(s):  
Eye Movements ◽  
Rem Sleep ◽  
Rapid Eye Movements ◽  
Pgo Waves

REM sleep burst neurons, PGO waves, and eye movement information

1983 ◽  
Vol 50 (4) ◽  
pp. 784-797 ◽  
Author(s):  
J. P. Nelson ◽  
R. W. McCarley ◽  
J. A. Hobson
Keyword(s):  
Eye Movements ◽  
Visual System ◽  
Eye Movement ◽  
Rem Sleep ◽  
Rapid Eye Movement Sleep ◽  
Generation System ◽  
Rapid Eye Movements ◽  
Midbrain Neurons ◽  
Burst Neuron ◽  
Pgo Waves

Pontogeniculooccipital (PGO) waves appeared almost simultaneously in both lateral geniculate nuclei (LGB), but in each case on had a larger amplitude and preceded the other by a few milliseconds. The larger, earlier wave is called the primary wave. Primary waves were found to appear with equal frequency in each LGB. During rapid eye movement sleep (REM sleep), LGB primary waves were ipsilateral to the direction of rapid eye movements. During REM sleep a group of cat midbrain neurons, which we call PGO burst cells, fired in stereotyped bursts at fixed latencies before ipsilateral primary waves, but they almost never fired bursts when the primary waves were contralateral. PGO burst neuron discharge also correlated with the direction of rapid eye movements during REM sleep. In wakefulness, PGO burst cells fired single spikes, not bursts, which had some correlation with LGB waves when averaged by computer. The results suggest that PGO burst cells are output elements in the PGO wave-generation system ad that PGO waves convey eye movement information to the sensory visual system in REM sleep. They also may have a role in the production of saccade-related waves in the visual system during wakefulness.

Quantitative Analysis of Abducens Neuron Discharge Dynamics During Saccadic and Slow Eye Movements

1999 ◽  
Vol 82 (5) ◽  
pp. 2612-2632 ◽  
Author(s):  
Pierre A. Sylvestre ◽  
Kathleen E. Cullen
Keyword(s):  
Eye Movements ◽  
Firing Rate ◽  
Eye Movement ◽  
Neuronal Activity ◽  
Smooth Pursuit ◽  
Slow Phase ◽  
Vestibular Nystagmus ◽  
Firing Rates ◽  
Rapid Eye Movements ◽  
Eye Velocity

The mechanics of the eyeball and its surrounding tissues, which together form the oculomotor plant, have been shown to be the same for smooth pursuit and saccadic eye movements. Hence it was postulated that similar signals would be carried by motoneurons during slow and rapid eye movements. In the present study, we directly addressed this proposal by determining which eye movement–based models best describe the discharge dynamics of primate abducens neurons during a variety of eye movement behaviors. We first characterized abducens neuron spike trains, as has been classically done, during fixation and sinusoidal smooth pursuit. We then systematically analyzed the discharge dynamics of abducens neurons during and following saccades, during step-ramp pursuit and during high velocity slow-phase vestibular nystagmus. We found that the commonly utilized first-order description of abducens neuron firing rates (FR = b + kE + rE˙, where FR is firing rate, E and E˙ are eye position and velocity, respectively, and b, k, and r are constants) provided an adequate model of neuronal activity during saccades, smooth pursuit, and slow phase vestibular nystagmus. However, the use of a second-order model, which included an exponentially decaying term or “slide” (FR = b + kE + rE˙ + uË − c[Formula: see text]), notably improved our ability to describe neuronal activity when the eye was moving and also enabled us to model abducens neuron discharges during the postsaccadic interval. We also found that, for a given model, a single set of parameters could not be used to describe neuronal firing rates during both slow and rapid eye movements. Specifically, the eye velocity and position coefficients ( r and k in the above models, respectively) consistently decreased as a function of the mean (and peak) eye velocity that was generated. In contrast, the bias ( b, firing rate when looking straight ahead) invariably increased with eye velocity. Although these trends are likely to reflect, in part, nonlinearities that are intrinsic to the extraocular muscles, we propose that these results can also be explained by considering the time-varying resistance to movement that is generated by the antagonist muscle. We conclude that to create realistic and meaningful models of the neural control of horizontal eye movements, it is essential to consider the activation of the antagonist, as well as agonist motoneuron pools.

Ventilatory responses to CO2 and lung inflation in tonic versus phasic REM sleep

1979 ◽  
Vol 47 (6) ◽  
pp. 1304-1310 ◽  
Author(s):  
C. E. Sullivan ◽  
E. Murphy ◽  
L. F. Kozar ◽  
E. A. Phillipson
Keyword(s):  
Eye Movements ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Minute Volume ◽  
Sleep State ◽  
Lung Inflation ◽  
Ventilatory Responses ◽  
Sustained Inflation ◽  
Per Se ◽  
Phasic Rem Sleep

Ventilatory responses to CO2 and to lung inflation were compared in four dogs during tonic and phasic segments of rapid-eye-movement (REM) sleep. Phasic REM sleep (P-REM) was identified by the presence of bursts of rapid eye movements, visible muscle twitchings, and frequent phasic discharges in the nuchal electromyogram. These features were absent during tonic REM sleep (T-REM). During P-REM the response of minute volume of ventilation (VI) to progressive hypercapnia (0.58 +/- 0.19 (l/min)/Torr, mean +/- SE) was significantly less than in slow-wave sleep (SWS) (1.40 +/- 0.14; P less than 0.05). In contrast, during T-REM the response (1.48 +/- 0.19) was similar to that in SWS. Similarly, during P-REM the duration of apnea (5.9 +/- 1.5 s) elicited by sustained inflation of the lungs with 1.0 liter of air, was significantly shorter than in SWS (25.8 +/- 0.8); in contrast, during T-REM the duration of apnea (17.8 +/- 3.6) was similar to that in SWS. The results indicate that previously described decreases in VI responses to CO2 and apneic responses to lung inflation during P-REM, compared to SWS, are related to the phasic phenomena of REM sleep, rather than to the REM sleep state per se.

scholarly journals Insights into paradoxical (REM) sleep homeostatic regulation in mice using an innovative automated sleep deprivation method

SLEEP ◽  
2020 ◽  
Vol 43 (7) ◽  
Author(s):  
Sébastien Arthaud ◽  
Paul-Antoine Libourel ◽  
Pierre-Hervé Luppi ◽  
Christelle Peyron
Keyword(s):  
Slow Wave ◽  
Rem Sleep ◽  
High Efficiency ◽  
Environmental Changes ◽  
Slow Wave Sleep ◽  
Paradoxical Sleep ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Homeostatic Regulation ◽  
External Modulation

Abstract Identifying the precise neuronal networks activated during paradoxical sleep (PS, also called REM sleep) has been a challenge since its discovery. Similarly, our understanding of the homeostatic mechanisms regulating PS, whether through external modulation by circadian and ultradian drives or via intrinsic homeostatic regulation, is still limited, largely due to interfering factors rendering the investigation difficult. Indeed, none of the studies published so far were able to manipulate PS without significantly altering slow-wave sleep and/or stress level, thus introducing a potential bias in the analyses. With the aim of achieving a better understanding of PS homeostasis, we developed a new method based on automated scoring of vigilance states—using electroencephalogram and electromyogram features—and which involves closed-loop PS deprivation through the induction of cage floor movements when PS is detected. Vigilance states were analyzed during 6 and 48 h of PS deprivation as well as their following recovery periods. Using this new automated methodology, we were able to deprive mice of PS with high efficiency and specificity, for short or longer periods of time, observing no sign of stress (as evaluated by plasma corticosterone level and sleep latency) and requiring no human intervention or environmental changes. We show here that PS can be homeostatically modulated and regulated while no significant changes are induced on slow-wave sleep and wakefulness, with a PS rebound duration depending on the amount of prior PS deficit. We also show that PS interval duration is not correlated with prior PS episode duration in the context of recovery from PS deprivation.

scholarly journals Neurons in the Nucleus papilio contribute to the control of eye movements during REM sleep

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
C. Gutierrez Herrera ◽  
F. Girard ◽  
A. Bilella ◽  
T. C. Gent ◽  
D. M. Roccaro-Waldmeyer ◽  
...  
Keyword(s):  
Eye Movements ◽  
Rem Sleep ◽  
Mammalian Brain ◽  
Eye Muscle ◽  
Genetic Ablation ◽  
Rapid Eye Movements ◽  
Motor Commands ◽  
Calbindin D28k ◽  
Contralateral Eye

AbstractRapid eye movements (REM) are characteristic of the eponymous phase of sleep, yet the underlying motor commands remain an enigma. Here, we identified a cluster of Calbindin-D28K-expressing neurons in the Nucleus papilio (NPCalb), located in the dorsal paragigantocellular nucleus, which are active during REM sleep and project to the three contralateral eye-muscle nuclei. The firing of opto-tagged NPCalb neurons is augmented prior to the onset of eye movements during REM sleep. Optogenetic activation of NPCalb neurons triggers eye movements selectively during REM sleep, while their genetic ablation or optogenetic silencing suppresses them. None of these perturbations led to a change in the duration of REM sleep episodes. Our study provides the first evidence for a brainstem premotor command contributing to the control of eye movements selectively during REM sleep in the mammalian brain.

Each distinct type of mental state is supported by specific brain functions

2000 ◽  
Vol 23 (6) ◽  
pp. 941-943 ◽  
Author(s):  
Claude Gottesmann
Keyword(s):  
Slow Wave ◽  
Mental State ◽  
Rem Sleep ◽  
Psychological Functioning ◽  
Slow Wave Sleep ◽  
Mental Content ◽  
Distinct Type ◽  
Inhibitory Processes ◽  
Brain Functions

Reflective waking mentation is supported by cortical activating and inhibitory processes. The thought-like mental content of slow wave sleep appears with lower levels of both kinds of influence. During REM sleep, the equation: activation + disinhibition + dopamine may explain the often psychotic-like mode of psychological functioning.[Hobson et al.; Nielsen; Revonsuo; Solms; Vertes & Eastman]

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