Self-deprivation of paradoxical sleep in cats

The phenomenon of paradoxical sleep (PS) self-deprivation has been detected and described. The self-deprivation is acquired just as a classical conditioned reflex during enforced PS deprivation both by water tank procedure and by the animal's awakenings in response to sensory stimuli or direct electric stimulation of activating structures of the midbrain and diencephalon, following the transition of slow-wave sleep to PS. In this situation the transition of the brain from one physiological state to another is a conditioned signal, and sensory stimulation or brain stimulation, resulting in arousal reaction, serves as an unconditioned stimulus. It is suggested that the detection and analysis of PS self-deprivation are of a great importance, on the one hand, for correct understanding of the functional significance of this physiological brain state, and, on the other hand, for accurate analysis and assessment of the dissociative processes, observed during PS deprivation and postdeprivation period.     

The role of the posterior hypothalamus in the regulation of paradoxical sleep

Posterior hypothalamus was found to take part in the inhibitory control of the paradoxical sleep executive mechanisms responsible for the ECoG desynchronisation and phasic events. Functional activity of the posterior hypothalamus seems to be at its lowest during the paradoxical sleep stage as characterised by phasic events and the ECoG desynchronisation, and increases during the stage with alpha-like activity in the ECoG and absence of phasic events, the latter having, probably, a "sentinel" function.     

Effects of dihydroergotoxine methane sulphonate (Redergine) on sleep in cats deprived of paradoxical sleep

Dihydroergotoxine methane sulphonate (DHET 1.0 mg/kg i.p.) was administered to cats deprived of paradoxical sleep (PS) for 72 h and 23 h of recovery sleep were recorded. During the first 12 h of recovery sleep slow-wave sleep (SWS) was significantly increased. There were no significant changes in the amounts of wakefulness (W), PS and several sleep indices. Analysis of the entire 23 h of recording period revealed no significant changes in any of the parameters studied. The results suggest that DHET has SWS enhancing property in the condition where "pressure" for PS was increased.     

Blood flow and pO2 in the posterior hypothalamus of cats during paradoxical sleep

In chronic experiments on cats it has been found by recording of the brain local blood flow (BLBF) and of oxygen tension (pO2) in the posterior and anterior hypothalamus, that at sleep phases alternation, the changes of these parameters are differently directed: during the paradoxical sleep the level of BLBF and pO2 oscillations frequency increased in the posterior hypothalamus and decreased in the anterior one. During slow-wave sleep opposite relations were observed. Opposite directions of changes of BLBF level and pO2 oscillations frequency in one and the same phase of sleep show that they are of local origin and must be determined by functional-metabolic shifts. In particular, the increase of BLBF level and frequency of pO2 oscillations must reflect a rise of posterior hypothalamus functional-metabolic activity during paradoxical sleep.     

Hypothermia and paradoxical sleep. I. Pontile cats without hypothalamo-hypophysis

Chronic pontile cats (without hypothalamo-hypophysis) were kept during 4 days at central T (TC) between 37.5 and 30.8 degrees C at stable ambiant T (TA) between 28.5 and 23 degrees C. The vasomotor index of the forepaw was chosen for studying change in vasomotricity. Small and slow variations of TA (+1.5 degrees C) around 27 degrees C were followed by thermoregulatory response since a progressive decrease of TA under 27 degrees C led to vasoconstriction and increase of TC while progressive increase of TA above 27 degrees C led to vasodilatation and decrease of TC. However rapid and large decrease of TA under 27 degrees C (24-23 degrees C) led to the expected hypothermia with decrease of TC but without vasoconstriction. Paradoxical sleep (PS) amounts were strongly correlated with TC. At TC above 35.5 degrees C PS was almost totally suppressed while it increased significantly under 35 degrees C (Q10 = 0.10). Under 35 degrees C at stable TC and TA, PS occurred with an endogenous circahoral rhythm which did not vary significantly between 35 and 32 degrees C. These results strongly suggest that in pontile cats, PS is both gated and regulated by TC, while TC is regulated by pontobulbar vasomotor systems in response to TA. The putative role of the ventro-lateral medulla, in controlling both vasomotricity, TC and the excitability of the locus coeruleus is discussed in relation with PS.     

Thermophysiology of the paradoxical sleep

Data on interactions between the paradoxical sleep (PS) and thermoregulation under thermo-comfortable and extreme conditions (in high and low temperatures, forced and spontaneous fasting, acclimation to cold and acclimation to natural winter conditions) are reviewed. The hypothesis of the PS role in synchronising and endogenous "kindling" of the visceral function ultradian rhythms is substantiated. Some new data are presented on entering torpor as a phenomenon of the "dramatic" neuronal plasticity.     

A voltametric study of the role of the noradrenaline innervation of the hippocampus in cats in paradoxical sleep

By the method of cyclic voltammetry with carbon fibrous electrodes the signal of 0.1 V was recorded from the dorsal hippocampus of male cats during natural sleep. Systemic injection of 50 mg of L-DOPA and 2.5 mg of isadrin did not influence the 0.1 V signal but the pyrroxan in a dose of 15 mg caused an increase of the signal amplitude. Parallel record of the EEG, myogram, oculogram and voltammogram showed that the 0.1 V signal, reflecting the level of alpha-adrenoreceptor norepinephrine content in the hippocampus increased in the first and last 1-2 minutes of the paradoxical sleep phase and was not stably recorded in the slow-wave phase and the middle part of the paradoxical phase of sleep. The conclusion is made that paradoxical sleep of cats consists of three parts. Initial and the final parts proceed against the background of the activity of the hippocampus alpha-adrenoreceptor norepinephrine innervation, triggering and stopping the basal phase of the paradoxical sleep, presumably activated by the serotonin innervation. On the basis of the present and previous studies the theory is suggested about the trigger function of the hippocampus and of the monoamines, innervating it, in the central mechanisms of conditioned behaviour and paradoxical sleep.     

Central regulation of temperature in hibernation and normothermia

Normothermic hibernators respond proportionally to both peripheral and brain temperature changes like other mammals. Their quantitative responsiveness to peripheral and brain temperature inputs are consistent with body-size relationships seen in other vertebrates. The basic temperature regulatory mechanisms seen in seasonal hibernators are not altered with season although certain response parameters, such as vasomotion, are not obvious in prehibernating marmots.     

Brainstem neurons responsible for postural, masseter or pharyngeal muscle atonia during paradoxical sleep in freely-moving cats

In this mini review, we summarize our findings regarding the brainstem neurons responsible for the postural, masseter, or pharyngeal muscle atonia observed during paradoxical sleep (PS) in freely moving cats. Both the pons and medulla contain neurons showing tonic activation selective to PS and atonia, referred to as PS/atonia-on-neurons. The PS/atonia-on neurons, characterized by their most slow conducting property and located in the peri-locus coeruleus alpha (peri-LCa) and adjacent LCa of the mediodorsal pontine tegmentum, play a critical executive role in the somatic and orofacial muscle atonia observed during PS. Slow conducting medullary PS/atonia-on neurons located in the nuclei reticularis magnocellularis (Mc) and parvocellularis (Pc) may play a critical executive role in the generation of, respectively, antigravity or orofacial muscle atonia during PS. In addition, either tonic or phasic cessation of activity of medullary serotonergic neurons may play an important role in the atonia of genioglossus muscles during PS via a mechanism of disfacilitation.     

Interdependence of learning and paradoxical sleep in the cat

The effect of learning sessions on the structure of the sleep-wakefulness cycle, as well as the effect of paradoxical sleep (PS) deprivation (PSD) following learning sessions, on the acquisition and extinction of instrumental alimentary reflexes to two feeders with sound discrimination, were studied on cats. The analysis of the data obtained led to following conclusions: The above learning sessions have no marked effect on the structure of the sleep-wakefulness cycle in the post-learning period, i.e. the percentage ratio of its phases is not altered by the increase of one of them. When PSD by non-emotional awakening is used, the number of PS onsets is not affected by learning sessions. This indicates that learning does not produce any considerable effect on the formation of PS need. PSD by non-emotional awakening following learning sessions does not retard the acquisition and extinction of the instrumental alimentary reflexes. The above data are interpreted as indicating that PS has no specific significance in memory trace consolidation during formation of long-term memory.     

Systemic or intracerebral injection of bovine neurointermediate lobe extracts may induce paradoxical sleep in insomnia induced by p-chlorophenylalanine in cats

Injections of Bovine neuro-intermediate lobe extracts, either subcutaneously (5 U), intraventricularly (20 mU) or directly in the vicinity of the nucleus magnocellularis of the medulla (1,3 mU) may induce paradoxical sleep in totally insomniac cats pretreated with P. chlorophenylalanine.     

Central circuitries for body temperature regulation and fever

Body temperature regulation is a fundamental homeostatic function that is governed by the central nervous system in homeothermic animals, including humans. The central thermoregulatory system also functions for host defense from invading pathogens by elevating body core temperature, a response known as fever. Thermoregulation and fever involve a variety of involuntary effector responses, and this review summarizes the current understandings of the central circuitry mechanisms that underlie nonshivering thermogenesis in brown adipose tissue, shivering thermogenesis in skeletal muscles, thermoregulatory cardiac regulation, heat-loss regulation through cutaneous vasomotion, and ACTH release. To defend thermal homeostasis from environmental thermal challenges, feedforward thermosensory information on environmental temperature sensed by skin thermoreceptors ascends through the spinal cord and lateral parabrachial nucleus to the preoptic area (POA). The POA also receives feedback signals from local thermosensitive neurons, as well as pyrogenic signals of prostaglandin E(2) produced in response to infection. These afferent signals are integrated and affect the activity of GABAergic inhibitory projection neurons descending from the POA to the dorsomedial hypothalamus (DMH) or to the rostral medullary raphe region (rMR). Attenuation of the descending inhibition by cooling or pyrogenic signals leads to disinhibition of thermogenic neurons in the DMH and sympathetic and somatic premotor neurons in the rMR, which then drive spinal motor output mechanisms to elicit thermogenesis, tachycardia, and cutaneous vasoconstriction. Warming signals enhance the descending inhibition from the POA to inhibit the motor outputs, resulting in cutaneous vasodilation and inhibited thermogenesis. This central thermoregulatory mechanism also functions for metabolic regulation and stress-induced hyperthermia.