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

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.

1979 ◽  
Vol 47 (6) ◽  
pp. 1304-1310 ◽  
Author(s):  
C. E. Sullivan ◽  
E. Murphy ◽  
L. F. Kozar ◽  
E. A. Phillipson

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.


1994 ◽  
Vol 71 (1) ◽  
pp. 95-109 ◽  
Author(s):  
S. Datta ◽  
J. A. Hobson

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)


2018 ◽  
Author(s):  
Giulio Bernardi ◽  
Monica Betta ◽  
Emiliano Ricciardi ◽  
Pietro Pietrini ◽  
Giulio Tononi ◽  
...  

AbstractAlthough the EEG slow wave of sleep is typically considered to be a hallmark of Non Rapid Eye Movement (NREM) sleep, recent work in mice has shown that slow waves can also occur in REM sleep. Here we investigated the presence and cortical distribution of low-frequency (1-4 Hz) oscillations in human REM sleep by analyzing high-density EEG sleep recordings obtained in 28 healthy subjects. We identified two clusters of low-frequency oscillations with distinctive properties: 1) a fronto-central cluster characterized by ∼2.5-3.0 Hz, relatively large, notched delta waves (so-called ‘sawtooth waves’) that tended to occur in bursts, were associated with increased gamma activity and rapid eye movements, and upon source modeling, displayed an occipito-temporal and a fronto-central component; and 2) a medial occipital cluster characterized by more isolated, slower (<2 Hz) and smaller waves that were not associated with rapid eye movements, displayed a negative correlation with gamma activity and were also found in NREM sleep. Thus, low-frequency oscillations are an integral part of REM sleep in humans, and the two identified subtypes (sawtooth and medial-occipital slow waves) may reflect distinct generation mechanisms and functional roles. Sawtooth waves, which are exclusive to REM sleep, share many characteristics with ponto-geniculo-occipital (PGO) waves described in animals and may represent the human equivalent or a closely related event while medio-occipital slow waves appear similar to NREM sleep slow waves.


1984 ◽  
Vol 42 (3) ◽  
pp. 232-241 ◽  
Author(s):  
Enaytolah Niakan ◽  
Tulio E. Bertorini ◽  
Helio Lemmi ◽  
Milton Medeiros ◽  
Richard Drewry ◽  
...  

Four members of a family with spinocerebellar degeneration and slow saccadic eye movements are described. Detailed electrophysiological studies revealed abnormalities of neurological pathways not apparent clinically. The patients had slow saccades as mesasured electrophysiologically, as well as absence of rapid eye movements (REM) despite REM stages of sleep. These studies suggest that although saccadic eye movement and REM are mediated through the pontine paramedian reticular formation, other characteristics of REM sleep are not necessarily mediated through the same neurons.


1966 ◽  
Vol 20 (4) ◽  
pp. 410-411 ◽  
Author(s):  
Richard B. Yules ◽  
John A. Ogden ◽  
Frederick P. Gault ◽  
Daniel X. Freedman

1977 ◽  
Vol 55 (2) ◽  
pp. 234-242 ◽  
Author(s):  
M. Rezek ◽  
V. Havlicek ◽  
L. Leybin ◽  
C. Pinsky ◽  
E. A. Kroeger ◽  
...  

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).


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
C. Gutierrez Herrera ◽  
F. Girard ◽  
A. Bilella ◽  
T. C. Gent ◽  
D. M. Roccaro-Waldmeyer ◽  
...  

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.


2020 ◽  
Vol 74 ◽  
pp. 341-342
Author(s):  
Maïlys Rupin-Mas ◽  
Isabelle Gourfinkel-An ◽  
Isabelle Arnulf

Author(s):  
Barbara E. Jones

Neurons distributed through the reticular core of the brainstem, hypothalamus, and basal forebrain and giving rise to ascending projections to the cortex or descending projections to the spinal cord promote the changes in cortical activity and behavior that underlie the sleep–wake cycle and three states of waking, NREM (slow wave) sleep, and REM (paradoxical) sleep. Forming the basic units of these systems, glutamate and GABA cell groups are heterogeneous in discharge profiles and projections, such that different subgroups can promote cortical activation (wake/REM(PS)-active) versus cortical deactivation (NREM(SWS)-active) by ascending influences or behavioral arousal with muscle tone (wake-active) versus behavioral quiescence with muscle atonia (NREM/REM(PS)-active) by descending influences. These different groups are in turn regulated by neuromodulatory systems, including cortical activation (wake/REM(PS)-active acetylcholine neurons), behavioral arousal (wake-active noradrenaline, histamine, serotonin, and orexin neurons), and behavioral quiescence (NREM/REM(PS)-active MCH neurons). By different projections, chemical neurotransmitters and discharge profiles, distinct cell groups thus act and interact to promote cyclic oscillations in cortical activity and behavior forming the sleep-wake cycle and states.


1987 ◽  
Vol 63 (4) ◽  
pp. 1463-1468 ◽  
Author(s):  
B. J. Koos ◽  
H. Sameshima ◽  
G. G. Power

Graded anemia was produced for 2 h in 10 unanesthetized fetal sheep by infusing plasma in exchange for fetal blood. This reduced the mean fetal hematocrits during the 1st h of anemia to 19.7 +/- 0.5% [control (C) = 28.2 +/- 1.1%] for mild anemia, 17.4 +/- 0.9% (C = 30.0 +/- 1.1%) for moderate anemia, and 15.1 +/- 1.0% (C = 29.2 +/- 1.3%) for severe anemia. The respective mean arterial O2 contents (CaO2) were 4.46 +/- 0.20, 3.89 +/- 0.24, and 3.22 +/- 0.19 ml/dl. Mean arterial PO2 was reduced significantly (by 2 Torr) only during moderate anemia, and mean arterial pH was decreased only during severe anemia. No significant changes occurred in arterial PCO2. Fetal tachycardia occurred during anemia. Mean arterial pressure was reduced by 2–3 mmHg during mild anemia; however, no significant blood pressure changes were observed for moderate or severe anemia. The incidence of rapid-eye movements and breathing activity was not affected by mild anemia, but the incidence of both was reduced significantly during moderate and severe anemia. It is concluded that 1) a reduction in CaO2 of greater than 2.48 +/- 0.22 ml/dl by hemodilution inhibits rapid-eye movements and breathing activity, and 2) the PO2 signal for inhibition does not come from arterial blood but from lower PO2 in tissue.


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