Paradoxical Sleep Deprivation In Rats Research Articles

Paradoxical sleep deprivation induces oxidative stress in the submandibular glands of Wistar rats.

Paradoxical sleep deprivation has been associated with impaired salivary secretion in rats. However, the mechanism that underlies this is not known. Therefore, this study assessed salivary and serum oxidative stress levels following paradoxical sleep deprivation in rats. Twenty-one male Wistar rats randomly divided into three groups of seven rats each as; Control (C); partialsleep-deprived (PSD); and total sleep-deprived (TSD) wereused. Malondialdehyde (MDA) concentration, Superoxide dismutase (SOD), and catalase activities were evaluated insaliva, serum, and submandibular glands after seven daysof sleep deprivation. Data were expressed as mean±standard error of the mean and analyzed using one-way ANOVA, Tukey HSD post hoc, and Pearson's correlation tests. Serum MDA levels were significantly higher in both the TSD and PSD groups compared to the control group whereas only the TSD group showed higher submandibular MDA levels compared to the PSD group and the control group. Submandibular SOD activity was significantly lower in both the TSD and PSD groups compared to the control group. Serum catalase activity was significantly lower in the TSD group only compared to the control group. These results have demonstrated for the first time that paradoxical sleep deprivation was associated with changes in the oxidant/antioxidant defense system in the submandibular salivary glands of male Wistar rats which may contribute to impairment in salivary secretion.

Is REM sleep a paradoxical state showing muscle atonia and a cortical activity similar to waking?

Michel Jouvet renamed REM sleep paradoxical sleep (PS) after his discovery that it displays an EEG similar to waking but with a complete muscle paralysis. To determine whether the cortical activation is similar during PS and waking, we recently identified at cellular level the populations of cortical neurons activated and displaying plasticity during waking and PS hypersomnia by means of functional neuroanatomy [3] . Our mapping clearly shows for the first time that only a small number of limbic structures are activated during PS in contrast to waking. These structures are the cortical amygdaloid nucleus, the anterior cingulate, retrosplenial and medial entorhinal cortices, the claustrum and the dentate gyrus (DG) [3] . Further, combining retrograde tracing, neurotoxic lesion and FOS immunostaining, we showed that neurons of the claustrum and from the lateral part of the supramammillary nucleus (SuML) are responsible for the activation of the cortical structures and the DG during PS [3] . We further recently showed using stimulation of the SuML/DG pathway using optogenetic induces an increase in theta power and frequency indicating that this pathway plays a role in theta. These surprising results pointed out for the first time that the claustrum and the SuML activate a subset of limbic cortical neurons specifically during PS in contrast to waking during which the aminergic, cholinergic and the hypocretin systems activate the cortex. We propose that the limbic cortical activation revealed in our study might play a key role in the previously reported beneficial effect of PS on learning and memory. Indeed, many studies clearly indicate that PS is instrumental for memory consolidation [1] . Further, it has recently been shown that PS deprivation in rats impairs consolidation of contextual fear conditioning [2] .

Paradoxical sleep deprivation in rats causes a selective reduction in the expression of type-2 metabotropic glutamate receptors in the hippocampus

Paradoxical sleep deprivation in rats is considered as an experimental animal model of mania endowed with face, construct, and pharmacological validity. We induced paradoxical sleep deprivation by placing rats onto a small platform surrounded by water. This procedure caused the animal to fall in the water at the onset of REM phase of sleep. Control rats were either placed onto a larger platform (which allowed them to sleep) or maintained in their home cage. Sleep deprived rats showed a substantial reduction in type-2 metabotropic glutamate (mGlu2) receptors mRNA and protein levels in the hippocampus, but not in the prefrontal cortex or corpus striatum, as compared to both groups of control rats. No changes in the expression of mGlu3 receptor mRNA levels or mGlu1α and mGlu5 receptor protein levels were found with exception of an increase in mGlu1α receptor levels in the striatum of SD rats. Moving from these findings we treated SD and control rats with the selective mGlu2 receptor enhancer, BINA (30mg/kg, i.p.). SD rats were also treated with sodium valproate (300mg/kg, i.p.) as an active comparator. Both BINA and sodium valproate were effective in reversing the manic-like phenotype evaluated in an open field arena in SD rats. BINA treatment had no effect on motor activity in control rats, suggesting that our findings were not biased by a non-specific motor-lowering activity of BINA. These findings suggest that changes in the expression of mGlu2 receptors may be associated with the enhanced motor activity observed with mania.

Leucine supplementation is anti-atrophic during paradoxical sleep deprivation in rats.

The purpose of this study was to identify sleep deprivation-induced atrophy and the muscle-specific fiber types affected and to determine the effects of leucine supplementation on atrophy and pertinent portions of the pathways of muscle protein synthesis and degradation in rats. A total of 46 Wistar rats were distributed in four groups: control (CTL), leucine supplementation (LEU), sleep deprivation (SD), and leucine supplementation + sleep deprivation (LEU + SD). Leucine supplementation was by gavage (1.35 g/kg/daily), and the animals were subjected to SD for 96 h. Testosterone and corticosterone concentrations, along with proteins involved in protein synthesis and degradation and proteasome activity levels, were measured in the gastrocnemius (GA) muscle. Myosin ATPase staining was used to evaluate the different muscle fibers. After sleep deprivation, GA muscle and body masses decreased in the SD group compared to the CTL, LEU, and LEU + SD groups. There was no difference between groups in type I fiber cross-sectional area (CSA). The CSAs for type IIa fibers were lower in the SD and LEU + SD groups vs. the CTL and LEU groups, while the IIb fiber CSA was lower in the SD group vs. the CSAs in all other groups. The phospho (p)-Akt levels were lower in the SD and LEU + SD groups vs. the CTL and LEU groups. The p-mTORC1 levels were higher in the LEU, SD, and LEU + SD groups vs. the CTL group. The p-p70S6k levels were higher in the LEU and LEU + SD groups; the 4E-BP1 levels were higher in the SD and LEU + SD groups compared to those in the CTL and LEU groups, and the p-4E-BP1 levels were higher in the LEU and SD groups compared to those in the CTL group and even higher in the LEU + SD group compared to those in the LEU and SD groups. Ubiquitinated proteins, LC3, and p62/SQSTM, and proteasome activity levels were higher in the SD and LEU + SD groups vs. the LEU and CTL groups. Sleep deprivation led to the atrophy of IIa and IIb muscle fibers; however, leucine supplementation prevented muscle loss and type IIb fiber atrophy.

Anesthetic propofol normalized the increased release of glutamate and γ-amino butyric acid in hippocampus after paradoxical sleep deprivation in rats

Objective: Multiple lines of evidence suggest that general anesthesia helps the recovery from sleep deprivation. However, little is known about the underlying neurochemical mechanisms. In the current study, we investigated the effect of anesthetic propofol on the release of glutamate (Glu) and γ-amino butyric acid (GABA) in the hippocampal CA1 region of rat with 24 h-paradoxical sleep deprivation (PSD).Methods: A guide cannula for microdialysis was inserted into the CA1 region of hippocampus in rats. At six days after cannula implantation, rats received 24 h-PSD by using the platform–water tank method. The rats were then subjected to natural sleep or propofol anesthesia (100 mg/kg, i.p.), respectively, after 24-h PSD. Microdialysis samples from hippocampus were collected before and at the end of PSD, and also at 1, 3, 6, and 8 h post-PSD. The concentrations of Glu and GABA in collected samples were determined by using high performance liquid chromatography.Results: The current study showed that 24 h-PSD significantly increased the release of Glu and GABA in the hippocampus in rats. In both natural sleep and propofol anesthesia groups, the upregulated Glu and GABA levels after PSD gradually decreased and returned to the baseline level by 8 h post-PSD.Conclusion: Our data indicate that propofol anesthesia promotes the restoration of disturbed excitatory and inhibitory neurotransmitter release in the hippocampus after PSD, similar to the beneficial effects of natural sleep. This finding suggests that propofol anesthesia may be a viable pharmacotherapeutic strategy for the treatment of certain sleep disorders that share similar mechanisms with PSD.

Cardiovascular alterations induced by acute paradoxical sleep deprivation in rats

Cardiovascular alterations induced by acute paradoxical sleep deprivation in rats

Inhibition of sympathetic activity by rilmenidine reverses angiotensin II-induced hypertension, blood pressure variability and cardiac remodeling

S SELECTED FOR PRESENTATION 14.4 Inhibition of sympathetic activity by rilmenidine reverses angiotensin II-induced hypertension, blood pressure variability and cardiac remodeling R. Sabharwal, R.N. El Accaoui, R.M. Weiss, M.K. Davis, F.M. Abboud, M.W. Chapleau Department of Internal Medicine, University of Iowa Veterans Affairs Medical Center, USA The relative contribution of increased sympathetic activity to angiotensin II (Ang II)-induced hypertension and end-organ damage is controversial. To determine the importance of the sympathetic nervous system, we examined whether sustained inhibition of sympathetic activity induced by intracerebroventricular infusion of rilmenidine (RIL) attenuates Ang II-induced hypertension, blood pressure variability and left ventricular (LV) remodeling. Blood pressure (BP) and heart rate (HR) were measured by telemetry in C57BL/6 mice (n= 7) and mice deficient in the antioxidant enzyme methionine sulfoxide reductase A (MsrA) (n= 8), before and during four weeks of Ang II infusion (1000 ng/kg/min, SC). LV end-diastolic volume (EDV), ejection fraction and mass were measured by echocardiography. Subgroups of mice were administered RIL (2.5 mg/kg/day, ICV, n = 4) over the last 2 weeks of Ang II infusion. Ang II infusion increased mean BP, BP variability, cardiac and vasomotor sympathetic tone, and LVEDV/mass ratio; and decreased cardiac vagal tone and spontaneous baroreflex sensitivity (sequence technique) (P b 0.05). All measures of dysfunction were exacerbated in MsrA−/− mice. As expected, RIL decreased sympathetic tone in all mice. Remarkably, RIL completely reversed Ang II-induced hypertension, BP variability, autonomic dysregulation, and LV remodeling in C57BL/6 andMsrA−/− mice (P b 0.05). RIL also increased (normalized) LV ejection fraction and locomotor activity in Ang II-infused MsrA−/− mice (P b 0.05). We conclude that Ang II-induced hypertension, BP variability and LV remodeling are critically dependent on increased sympathetic activity. The results strongly support therapeutic targeting of the brain to inhibit sympathetic activity in hypertension. (HL14388, VA). doi:10.1016/j.autneu.2015.07.320 14.5 Brain and renal alterations following denervation of ischemic kidney in renovascular hypertension E.E. Nishi, C.T. Bergamaschi, G.N. Gomes, J.C. Perry, G.S. Lincevicius, R.R. Campos Physiology Dpt., Universidade Federal de Sao Paulo, Brazil Psychobiology Dpt., Universidade Federal de Sao Paulo, Brazil Our aim was to investigate whether renal nerves play a role in the renal injury process and modulation of AngII receptors expression in the central nuclei and kidneys in renovascular hypertension. Denervation of clipped kidney (RD: visible bundles were dissected + 10% phenol) was performed in Wistar male rats (n = 5/group) 4–5 weeks after clip implantation (gap width: 0.2 mm). Ten days after RD, blood pressure (BP) was significantly reduced in the 2 K-1C rats. AT1R and AT2R upregulation within the rostral ventrolateral medulla (RVLM) and paraventricular nucleus of the hypothalamus (PVN) in the 2 K-1C group was normalized after RD. No change in the expression of either AngII receptor was found within the nucleus of the tractus solitarius (NTS). Following RD, there was no change in plasma renin activity in control and 2 K-1C rats. In order to distinguish the effects of RD from the reduction in BP, 2 K-1C rats were treated orally with hydralazine (25 mg/kg/day for seven consecutive days). Hydralazine significantly reduced BP and AT1R within the PVN in the 2 K-1C rats, but there were no changes in AT1R or AT2R within the RVLM and NTS. Following RD, renal injury was attenuated in both ischemic and contralateral kidneys of hypertensive rats, although hydralazine decreased injury only in the contralateral kidney. These results demonstrate that the renal nerves may modulate AngII receptors within the RVLM and renal injury in the ischemic kidney independent of BP and plasma renin activity in the 2 K-1C model of arterial hypertension. Supported by FAPESP and CNPq. doi:10.1016/j.autneu.2015.07.321 Symposium 15: Sleep and autonomic nervous system: At the crossroad between health and disease 15.1 Cardiovascular alterations induced by acute paradoxical sleep deprivation in rats

The Pronociceptive Effect of Paradoxical Sleep Deprivation in Rats: Evidence for a Role of Descending Pain Modulation Mechanisms.

The mechanisms underlying the pronociceptive effect of paradoxical sleep deprivation (PSD) are not known. In this study, we asked whether PSD increases tonic nociception in the formalin test, decreases the antinociceptive effect of morphine administered into the periaqueductal gray matter (PAG), and disrupts endogenous descending pain modulation. PSD for either 24 or 48 h significantly increased formalin-induced nociception and decreased mechanical nociceptive paw withdrawal threshold. The maximal antinociceptive effect induced by morphine (0.9-9 nmol, intra-PAG) was significantly decreased by PSD. The administration of a low dose of the GABAA receptor antagonist, bicuculline (30-300 pmol, intra-PAG), decreased nociception in control rats, but not in paradoxical-sleep-deprived ones. Furthermore, the administration of the cholecystokinin (CCK) 2 receptor antagonist, YM022 (0.5-2 pmol) in the rostral ventral medulla (RVM), decreased nociception in paradoxical-sleep-deprived rats but not in control ones. While a dose of the CCK 2 receptor agonist, CCK-8 (8-24 pmol intra-RVM), increased nociception in control rats, but not in paradoxical-sleep-deprived ones. In addition, the injection of lidocaine (QX-314, 2%, intra-RVM) decreased nociception in sleep-deprived rats, but not in control rats, while the lesion of the dorsolateral funiculus prevented the pronociceptive effect of PSD. Finally, PSD significantly increased c-Fos expression in the RVM. Therefore, PSD increases pain independently of its duration or of the characteristic of the nociceptive stimulus and decreases morphine analgesia at the PAG. PSD appears to increase pain by decreasing descending pain inhibitory activity and by increasing descending pain facilitatory activity.

Sleep loss changes neuropeptidase expression and activty in rat brain (876.3)

The effect of sleep deprivation on proteolytic activity in the central nervous system has not been frequently addressed in the literature. We have started to study the changes on peptidase activities in animal models of paradoxical sleep deprivation (PSD), mainly focusing on metallopeptidases like thimet oligopeptidase (EP24.15) known to process neuropeptides. In the present study, we demonstrated that PSD in rats induces changes both in the expression and activity of EP24.15 in the male rat hypothalamus and striatum tissue extracts. In the hypothalamus, the significant decrease in activity and mRNA levels, after PSD, was only totally reversed after 96h of sleep recovery. In the striatum, albeit significative, changes in mRNA and activity do not parallel changes on protein content. Neurotensin, GnRH, dynorphins, enkephalins, orphanin/nociceptin are among the many neuropeptides whose balance can be modified by the modifications on EP24.15 activity and can be, at least partially, related with many of the physiological changes observed in PSD and during the sleep recovery periods.Grant Funding Source: Supported by FAPESP, CNPq and AFIP

Cardiovascular function alterations induced by acute paradoxical sleep deprivation in rats

Sleep loss has been implicated in triggering the hypertension. The goal of the present study was investigated the possible mechanisms underlying cardiovascular alterations after acute paradoxical sleep deprivation (PSD). Male Wistar rats were assigned in two experimental groups: (1) control and (2) PSD for 24 h using the modified single platform method. Paradoxical sleep deprived rats exhibited higher blood pressure, heart rate (HR) and impaired baroreceptor sensitivity. After pharmacological autonomic double blockade (propranolol and methylatropine administration), intrinsic heart rate was decreased after PSD. The PSD rats showed a reduction in the vagal tone without affecting sympathetic tone. Isoproterenol administration (0.001, 0.01 and 1 µg/kg) induced an increase in ΔHR responses in PSD group. Electrocardiographic analysis in response to β-adrenergic stimulation indicated that PSD contributed to ventricular cardiac arrhythmias. Our findings suggest that acute paradoxical sleep loss induce cardiovascular alterations, autonomic imbalance accompanied by impaired baroreflex sensitivity and increased arrhythmia susceptibility.

Aerobic exercise attenuates inhibitory avoidance memory deficit induced by paradoxical sleep deprivation in rats

The deleterious effects of paradoxical sleep deprivation (SD) on memory processes are well documented. Physical exercise improves many aspects of brain functions and induces neuroprotection. In the present study, we investigated the influence of 4 weeks of treadmill aerobic exercise on both long-term memory and the expression of synaptic proteins (GAP-43, synapsin I, synaptophysin, and PSD-95) in normal and sleep-deprived rats. Adult Wistar rats were subjected to 4 weeks of treadmill exercise training for 35min, five times per week. Twenty-four hours after the last exercise session, the rats were sleep-deprived for 96h using the modified multiple platform method. To assess memory after SD, all animals underwent training for the inhibitory avoidance task and were tested 24h later. The aerobic exercise attenuated the long-term memory deficit induced by 96h of paradoxical SD. Western blot analysis of the hippocampus revealed increased levels of GAP-43 in exercised rats. However, the expression of synapsin I, synaptophysin, and PSD-95 was not modified by either exercise or SD. Our results suggest that an aerobic exercise program can attenuate the deleterious effects of SD on long-term memory and that this effect is not directly related to changes in the expression of the pre- and post-synaptic proteins analyzed in the study.

Neurochemical and electrophysiological changes induced by paradoxical sleep deprivation in rats

The present study aims to investigate the effects of paradoxical sleep deprivation (PSD) on the waking EEG and amino acid neurotransmitters in the hippocampus and cortex of rats. Animals were deprived of paradoxical sleep for 72 h by using the multiple platform method. The EEG power spectral analysis was carried out to assess the brain's electrophysiological changes due to sleep deprivation. The concentrations of amino acid neurotransmitters were assessed in the hippocampus and cortex using HPLC. Control data showed slight differences from normal animals in the delta, theta and alpha waves while an increase in the beta wave was obtained. After 24 h of PSD, delta relative power increased and the rest of EEG wave's power decreased with respect to control. After 48 h and 72 h the spectral power analysis showed non-significant changes to control. The amino acid neurotransmitter analysis revealed a significant increase in cortical glutamate, glycine and taurine levels while in the hippocampus, glutamate, aspartate, glutamine and glycine levels increased significantly. Both the waking EEG and neurotransmitter analyses suggest that PSD induced neurochemical and electrophysiological changes that may affect brain proper functionality.

Effects of cocaine, methamphetamine and modafinil challenge on sleep rebound after paradoxical sleep deprivation in rats

Sleep loss is both common and critically relevant to our society and might lead to the abuse of psychostimulants such as amphetamines, cocaine and modafinil. Since psychoactive substance abuse often occurs within a scenario of sleep deficit, the purpose of this investigation was to compare the sleep patterns of rats challenged with cocaine (7 mg/kg, ip), methamphetamine (7 mg/kg, ip), or modafinil (100 mg/kg, ip) subsequent to paradoxical sleep deprivation (PSD) for 96 h. Our results show that, immediately after 96 h of PSD, rats (10 per group) that were injected with a psychostimulant presented lower percentages of paradoxical sleep compared to those injected with saline (P < 0.01). Regarding slow wave sleep (SWS), rats injected with psychostimulants after PSD presented a late rebound (on the second night subsequent to the injection) in the percentage of this phase of sleep when compared to PSD rats injected with saline (P < 0.05). In addition, the current study has produced evidence of the characteristic effect of each drug on sleep architecture. Home cage control rats injected with modafinil and methamphetamine showed a reduction in SWS compared with the saline group. Methamphetamine affected sleep patterns most, since it significantly reduced paradoxical sleep, SWS and sleep efficiency before and after PSD compared to control (P < 0.05). Cocaine was the psychostimulant causing the least changes in sleep pattern in relation to those observed after saline injection. Therefore, our results suggest that abuse of these psychostimulants in a PSD paradigm aggravates their impact on sleep patterns.

Distinct behavioral and neurochemical alterations induced by intermittent hypoxia or paradoxical sleep deprivation in rats

The current study investigated the effects of paradoxical sleep deprivation and intermittent hypoxia by examining whether a combination of the two would induce anxiety-like alterations in behavior. The neurochemical effects of these manipulations were investigated by measuring cortical, striatal and hippocampal monoamine concentrations. Wistar Hannover rats were submitted to subchronic (3 days) intermittent hypoxia exposure (alternating cycles of 2 min room air–2 min 10% O 2 from 0700–1900 h) and paradoxical sleep deprivation using the single platform method. Rats were randomly assigned to four different protocols: 1) control, 2) intermittent hypoxia during the light period (12 h/day), 3) paradoxical sleep deprivation (24 h/day), and 4) intermittent hypoxia combined with paradoxical sleep deprivation. Rats subjected to intermittent hypoxia showed no modification in the behavioral or neurochemical parameters assessed. Although paradoxical sleep deprivation did not produce alterations in anxiety-like behavior, the rats did increase exploratory activity in the elevated plus-maze. Moreover, a significant increase in striatal epinephrine and hippocampal homovanilic acid (HVA) concentrations was found in the paradoxical sleep deprivation groups, but not in the intermittent hypoxia/paradoxical sleep deprivation group. Of note, both paradoxical sleep deprivation and intermittent hypoxia/paradoxical sleep deprivation groups showed an increase in plasma corticosterone concentration. These results suggest that paradoxical sleep deprivation induces behavioral alterations, and these abnormalities may reflect altered neurotransmission in the brain. When paradoxical sleep deprivation was combined with intermittent oxygen depletion, the behavioral and biochemical parameters were comparable to those of control rats.

L0027 Renal sympathetic activation induced by paradoxical sleep deprivation in rats

L0027 Renal sympathetic activation induced by paradoxical sleep deprivation in rats

P303 Differential sympathetic activation induced by intermittent hypoxia associated to paradoxical sleep deprivation in rats

P303 Differential sympathetic activation induced by intermittent hypoxia associated to paradoxical sleep deprivation in rats

Vocalization thresholds related to noxious paw pressure are decreased by paradoxical sleep deprivation and increased after sleep recovery in rat

The aim of this study was to assess the effect of paradoxical sleep deprivation (PSD) and sleep recovery on the vocalization threshold in rats submitted to a mechanical noxious stimulus. Sixteen male Wistar rats were randomly assigned in two groups: controls (n=8), paradoxical sleep deprived rats (n=8). PSD was performed using the ‘inverted flower pot’ technique. Paw pressure test was used to assess the sensitivity to mechanical noxious stimulus (vocalization threshold). The experiment was divided into three periods: baseline (day 1, day 2), PSD (day 3, day 4, day 5) and recovery (day 6, day 7, day 8, day 9). After 48 and 72 h of PSD, the vocalization thresholds decreased significantly in comparison to the control rats (day 4: 245±21 vs. 303±20 g, P=0.05; day 5: 256±17 vs. 324±22 g, P=0.02). In PSD group, relative to controls, vocalization thresholds increased significantly after 48, 72, and 96 h of recovery sleep periods (day 7: 378±24 vs. 307±8 g P=0.01; day 8: 384±27 vs. 316±23 g, P=0.02; day 9: 395±24 vs. 328±15 g, P=0.02). Vocalization thresholds on day 6 were not significantly different in both groups (375±20 vs. 324±24 g, P=0.08). In conclusion, experimental PSD in rats induces a significant decrease in vocalization threshold to mechanical noxious stimulus, which is totally reversed during the sleep recovery period.

Absence of oxidative stress following paradoxical sleep deprivation in rats

Paradoxical sleep deprivation was performed on rats using platform technique to investigate the oxidative process associated with it. Levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), total glutathione (GSH) and malondialdehyde production were measured in brain of rats under control conditions (C) and those on single large platforms (SLP), multiple large platforms (MLP), single small platforms (SSP) and multiple small platforms (MSP) groups. SOD, CAT and GPx brain activity and malondialdehyde production were not modified by any of the procedures. Brain GSH, however, was significantly reduced in both SSP and SLP groups. These results suggest that paradoxical sleep deprivation per se is not associated with oxidative damage. The observed alterations could be attributed to factors such as immobilization and social isolation present in the single platform techniques.

Behavioral evaluation of the stress induced by the platform method for short-term paradoxical sleep deprivation in rats

To evaluate whether the results of short-term PSD (Paradoxical Sleep Deprivation) using the platform method can be influenced by stress, changes in body weight and in behavioral indices (food and water intake and ambulation and defecation in an open field) were measured in rats after each of four 5-hour sessions of confinement to small or large platforms. The animals of the two platform groups when compared to animals kept in home cages showed a similar decrease in body weight which was significant only after the first day of treatment, while no changes in the other measures were observed. It is concluded that 1) the effects of stress induced by short-term confinement to platforms do not seem to be a remarkable confounding factor in short-term PSD studies and 2) large platforms can be used both as an adequate stress control for small platforms and as a means of adapting the animals to the method.

Photically evoked potentials in the visual cortex following paradoxical sleep deprivation in rats

Immediately following 72 hr of paradoxical sleep (PS) deprivation, the P3-N3 amplitude of the photically evoked response in the visual cortex was measured in waking rats. PS deprivation was achieved instrumentally by one of three different techniques: the classical platform, the multiple platform, or the pendulum technique. For each of the techniques a control condition was run additionally. The PS deprivation effect consisted of a decrement in the P3-N3 amplitude, which was interpreted as indicating an increase in tonic arousal having a depressing influence on cortical excitability. Concomitantly, a relatively large technique effect occurred, in which the difference between the two platform techniques on the one hand, and the pendulum technique on the other, was most apparent. The same factors did not influence behavioural activity taking place during the presentation of photic stimulation, but did during the preceding 5 min adaptation period. Although the present findings are in contrast with previous reports in animals, they may not be inconsistent with the basic idea of the neural excitability hypothesis of PS.