Effects of temperature and volume on intraperitoneal saline-induced changes in blood pressure,nociception, and neural activity in the rostroventral medulla

ON and OFF cells of the rostral ventromedial medulla are hypothesized to modulate nociception with ON cells facilitating pain and OFF cells inhibiting pain. The current study analyzed the effects of intraperitoneal saline at different volumes and temperatures on nociception (tail flick reflex), blood pressure, and the activity of ON and OFF cells in lightly anesthetized rats. At large volumes (20 cc/kg), room temperature saline excited 7/11 ON cells and inhibited 10/12 OFF cells for 2-5 min. In contrast, large volumes (20 cc/kg) of body temperature saline (37 degrees C) excited only 1/10 ON cells and inhibited only 3/13 OFF cells, and small volumes (1-2 cc/kg) of room temperature saline excited only 3/10 ON cells and inhibited only 4/11 OFF cells. Tail flick latency increased following saline administration at large volumes with a significant effect of time, but not temperature. The excitation of ON cells and inhibition of OFF cells indicate that cold intraperitoneal saline could be painful and the increase in tail flick latency may indicate a diffuse noxious inhibitory control. It is also possible that the changes in ON and OFF cell activity caused a hyperalgesia that was masked by a simultaneous hypoalgesia that was mediated independent of the ON and OFF cells. Because intraperitoneal saline may produce pain or hyperalgesia, care should be used when saline is used experimentally or clinically.     

Comparison of the effects of central administration of serine and glycine on body temperature of the rabbit

When serine, a precursor of taurine, was injected into the lateral cerebral ventricle (ICV), it caused dose-related decreases in rectal temperature of rabbits in a cold environment (10°C) but had little effect in a thermoneutral environment or in the heat (30°C). Induction of fever by IV leukocytic pyrogen was inhibited by serine given ICV in a single injection, in two injections 30 min apart, or when infused for one hour in a thermoneutral environment; a single injection also inhibited fever in the heat. Reduction of body temperature in the cold and prevention of fever development in a thernoneutral environment were associated with vasodilatation of the ears; the inhibition of fever development in the heat, with suppression of vasoconstriction. The hyperthermic response to ICV PGE₂ (500 ng) was also inhibited by pretreatment with serine in both thermoneutral and hot environments. When serine and taurine were injected together ICV in a cold environment, the reductions in body temperature were consistent with an additive action of the two amino acids. The increased effects of acute serine injections over infusions of even greater amounts of the amino acid suggest that large doses of serine can influence early inward transport of endogenous pyrogen. Serine appears to inhibit activity in central pathways which mediate both heat production and heat conservation, possibly at the same receptor sites as taurine. Unlike taurine, however, serine infusion does not augment and prolong fever when infusion is stopped and it is unlikely that this amino acid influences inactivation of endogenous pyrogen that reaches the brain.     

Contrasting effects of E type prostaglandin (EP) receptor agonists on core body temperature in rats

Prostaglandin E2 (PGE2) is thought to be a principal fever mediator. There are four subtypes of PGE (EP) receptors, EP1-EP4. We investigated which EP receptors mediate PGE2-induced hyperthermia by injecting selective EP receptor agonists into the rat lateral cerebral ventricle under unrestrained condition. ONO-DI-004, an EP1 receptor agonist, increased the core temperature (T(c)) in a dose-dependent manner (1.6+/-0.1 degrees C at 20 nmol, with the peak 30 min after injection) with a time course similar to PGE2-induced hyperthermia. ONO-AE1-259-01 (20 nmol), an EP2 receptor agonist, did not change the T(c). ONO-AE-248 (20 nmol), an EP3 receptor agonist, also increased the T(c). However, the peak effect was delayed (1.2+/-0.2 degrees C, 50 min after injection) compared to PGE2. In contrast, ONO-AE1-329, an EP4 receptor agonist, decreased the T(c). These findings suggest that the EP1, EP3, and EP4 receptors all may contribute to the thermoregulatory response to PGE2, but each may have a different role.     

Dissociation between the effects of interleukin-1 on excitotoxic brain damage and body temperature in the rat

The cytokine interleukin-1beta (IL-1beta) mediates and exacerbates excitotoxic brain damage in the rat striatum. Co-injection of the selective glutamate receptor agonist alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (S-AMPA) with human recombinant IL-1beta (hrIL-1beta) in the striatum of rats results in both local (striatal) damage and extensive, distant neuronal death in the cortex. The objective of the present study was to investigate the mechanisms underlying IL-1beta actions on excitotoxic damage, and to determine whether this effect of IL-1beta, a potent pyrogen, is due to modification of body temperature. Striatal infusion of S-AMPA (7.5 nmol) in anaesthetised rats produced localised striatal damage. Intrastriatal co-infusion of hrIL-1beta (10 ng) with S-AMPA caused similar striatal damage, but also produced extensive cortical damage, together with a modest increase in body temperature (0.9 degrees C) compared to rats infused with S-AMPA alone. Infusion of S-AMPA into the striatum, together with intracerebroventricular (i.c.v.) injection of hrIL-1beta, produced a similar rise in temperature to striatal co-infusion of S-AMPA and hrIL-1beta, but resulted in only local (striatal) neuronal damage, that was similar to that caused by striatal infusion of S-AMPA alone. These data suggest that the effects of IL-1beta on AMPA-receptor mediated neuronal damage in the striatum can be dissociated from its pyrogenic effects on body temperature.     

Increased expression of mRNA encoding interleukin-1beta and caspase-1, and the secreted isoform of interleukin-1 receptor antagonist in the rat brain following systemic kainic acid administration

Kainic acid, an analogue of glutamate, injected systemically to rats evokes seizures that are accompanied by nerve cell damage primarily in the limbic system. In the present study, we have analyzed the temporal profile of the expression of the cytokines interleukin-1beta (IL-1beta) and IL-1 receptor antagonist (IL-1ra), and the related IL-1beta-converting enzyme (ICE/caspase-1), in different regions of the rat brain in response to peripheral kainic acid administration (10 mg/kg, i.p.). In situ hybridization histochemistry experiments revealed that IL-1beta mRNA-expressing cells, morphologically identified as microglial cells, were mainly localized to regions showing pronounced neuronal degeneration; hippocampus, thalamus, amygdala, and certain cortical regions. The strongest expression of IL-1beta mRNA was observed after 12 hr in these regions. A weak induction of the IL-1beta mRNA expression was observed already at 2 hr. Similar results were obtained by RT-PCR analysis, showing a significantly increased expression of IL-1beta mRNA in the hippocampus and amygdala after 12 hr. In addition, RT-PCR analysis revealed that IL-1ra mRNA, and specifically mRNA encoding the secreted isoform of IL-1ra (sIL-1ra), was strongly induced in the hippocampus and amygdala at 12 and 24 hr post-injection. RT-PCR analysis of mRNA encoding caspase-1 showed a significantly increased expression in the amygdala after 12 hr. In conclusion, in response to systemic kainic acid injection IL-1beta mRNA is rapidly induced and followed by induction of IL-1ra mRNA and caspase-1 mRNA, supporting a role of the IL-1 system in the inflammatory response during excitotoxic damage.     

Dissociation of hyperalgesia from fever following intracerebroventricular administration of interleukin-1beta in the rat

Interleukin-1beta (IL-1beta) is a cytokine that contributes to the hyperalgesia, inactivity, and fever associated with illness. These three components of the illness response occur simultaneously following peripheral administration of IL-1beta. The objective of the present study was to determine whether hyperalgesia, inactivity, and fever correspond following central administration. Rats were injected with IL-1beta (0.05 pg-50 ng/10 microl) into the lateral ventricle and core body temperature and activity were assessed for 5.5 h using radio telemetry while rats remained in their home cage. Rats were removed from the cage periodically to assess nociception by measuring the latency for hindpaw withdrawal to radiant heat. The two highest doses of IL-1beta (5 and 50 ng) caused an increase in core body temperature and a decrease in activity beginning 105 min following administration. No change in nociception was evident at any time after administration of IL-1beta regardless of dose. These data indicate that the hyperalgesia associated with fever is triggered by a peripheral, not a central action of IL-1beta, presumably by activation of vagal afferents.     

Single neuron activity changes to interleukin-1beta in the orbitofrontal cortex of the rat

The orbitofrontal cortex (OBF) is known to play important roles in various regulatory processes. Our preliminary behavioral studies showed homeostatic alterations after orbitofrontal cortical microinjection of interleukin-1beta (IL-1beta) in the rat. To elucidate whether the above alterations were due to direct neuronal action of the cytokine, extracellular single neuron activity was recorded in the OBF of anesthetized rats by means of tungsten fiber multibarreled glass microelectrodes during microelectrophoretic administration of IL-1beta. More than half (56%) of all cells tested changed in firing rate in response to IL-1beta. Approximately 90% of these cytokine-modulated neurons were also sensitive to microelectrophoretically applied d-glucose, that is, proved to be the elements of the central glucose-monitoring neural network. The present findings demonstrate that IL-1beta can exert direct modulatory role on neurons in the OBF.     

Anatomic patterns of FOS immunostaining in rat brain following systemic endotoxin administration

To identify brain neurons that participate in the acute phase response, rat brains were examined immunocytochemically for Fos protein following the intravenous administration of bacterial endotoxin (lipopolysaccharide, LIPS). Two to three hours after the injection of LPS, 150 μg/kg body weight, to adult male Long-Evans rats, a consistent anatomic pattern of Fos immunostained cell nuclei is seen. In the brain stem, prominant Fos immunostaining is induced in tyrosine hydroxylase immunoreactive neurons of the caudal ventral-lateral medulla (the A1 cell group), in both tyrosine hydroxylase positive and negative neurons of nu. tractus solitarius, in the parabrachial nu., and in a few neurons of the locus ceruleus. In the hypothalamus, endotoxin induces Fos expression in magnocellular neurons of the paraventricular and supraoptic nuclei and intemuclear cell groups. A higher percentage of oxytocin-immunoreactive cells is double labeled for Fos nuclear immunostaining than vasopressin-immunoreactive cells. A minority of somatostatin immunoreactive periventricutar hypothalamic neurons are Fos positive. Other hypothalamic nuclei that contain endotoxin-induced Fos nuclear immunostaining include the parvocellular neurons of the paraventricular nu., the dorsomedial and arcuate nuclei, the lateral hypothalamus, the dorsal hypothalamic area (zona incerta), and the median nucleus of the preoptic area. LPS induces numerous Fos-positive neurons in regions known to respond to a variety of stressful stimuli; these regions include the preoptic area, bed nucleus of the stria terminalis, lateral septum, and the central and medial nuclei of the amygdala. Moreover, Fos nuclear immunostaining is seen in neurons of circumventricular organs: the organum vasculosum of the lamina terminalis, the subfomical organ, and the area postrema. The maximum intensity of Fos nuclear immunostaining occurs 2–3 h after endotoxin administration and declines thereafter. It is attenuated by pretreatment with indomethacin, 25 mg/kg body weight SC, or dexamethasone, l mg/kg III. These observations are consistent with the participation of a variety of brain neuronal systems in the acute phase response and elucidate the functional neuroanatomy of that response at the cellular level.     

NMDA and quisqualate modulation of visceral nociception in the rat

The effects of acid (NMDA; 100 fmol-1 nmol) or quisqualic acid (QA; 10 pmol-10 nmol) on visceromotor and pressor responses to noxious colorectal distention (CRD; 40 mmHg, 20 s duration, interstimulus interval: 4 min) were studied in awake rats. Lesser doses of NMDA (100 fmol - 1 pmol) administered intrathecally (i.t.) to the lumbar spinal cord produced a dose-dependent facilitation of visceromotor as well as pressor responses to CRD (maximum with 1 pmol NMDA at 1 min). The greatest dose tested (1 nmol) attenuated these responses (maximum at 1 min) and also produced a caudally-directed biting and scratching behavior accompanied by vocalizations. NMDA did not produce any of the above effects when administered i.t. to the thoracic spinal cord. I.t. pretreatment with the NMDA receptor antagonist, -2-amino-5-phosphonovaleric acid ( -APV; 1 pmol), which produced no change in baseline activity or control responses, blocked all NMDA-produced effects in a reversible manner. QA produced dose-dependent inhibitory effects on visceromotor as well as pressor responses to noxious CRD when given i.t. to the lumbar spinal cord but not on administration to the thoracic spinal cord. Three nmol QA produced maximum inhibition at 2 min after administration and also produced caudally-directed biting and scratching. All of the QA-produced effects were reversibly blocked by i.t. pretreatment with the non-NMDA receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX; 3 nmol), which produced no change in baseline activity or control responses. We also examined the effects of NMDA and QA on responses to graded intensities of CRD. One pmol NMDA selectively facilitated visceromotor responses to CRD at distention pressures of 40 and 80 mmHg but not at 20 mmHg. In contrast, 3 nmol QA inhibited visceromotor responses to CRD at all intensities tested. In summary, these data suggest that activation of NMDA and non-NMDA receptors in the spinal cord differentially modulates visceral nociceptive input. Spinal segmental NMDA receptor activation produces selective facilitation of visceral nociceptive processing at noxious intensities of stimulation and may thereby contribute to central mechanisms underlying visceral hyperalgesia.     

The effects of prostaglandin E2 on the firing rate activity of thermosensitive and temperature insensitive neurons in the ventromedial preoptic area of the rat hypothalamus

In response to an immune system challenge with lipopolysaccharide (LPS), recent work has shown that Fos immunoreactivity is displayed by neurons in the ventromedial preoptic area of the hypothalamus (VMPO). In addition, neurons in this region show distinct axonal projections to the anterior perifornical area (APFx) and the paraventricular nucleus (PVN). It has been hypothesized that neurons within the VMPO integrate their local responses to temperature with changes in firing activity that result from LPS induced production of prostaglandin E(2) (PGE(2)). This may be an important mechanism by which the set-point regulation of thermoeffector neurons in the APFx and PVN is altered, resulting in hyperthermia. To characterize the firing rate activity of VMPO neurons, single-unit recordings were made of neuronal extracellular activity in rat hypothalamic tissue slices. Based on the slope of firing rate as a function of tissue temperature, neurons were classified as either warm sensitive or temperature insensitive. Neurons were then treated with PGE(2) (200 nM) while tissue temperature was held at a constant level ( approximately 36 degrees C). The majority of temperature insensitive neurons responded to PGE(2) with an increase in firing rate activity, while warm sensitive neurons showed a reduction in firing rate. This suggests that both warm sensitive and temperature insensitive neurons in the VMPO may play critical and contrasting roles in the production of a fever during an acute phase response to infection.     

Long-term blockade of μ-opioid receptors suggests a role in control of ingestive behaviour, body weight and core temperature in the rat

Chronic subcutaneous infusion with a low dose (0.5 mg/kg/h) of naloxone via minipumps blocked the antinociceptive action of the μ-agonist, morphine, without affecting that of the κ-agonist, U50488H. This dose resulted in a transient suppression in the rate of body weight gain and a sustained reduction in daily food intake (FI) and water intake (WI): this decrease was seen in both the light and dark phases. Naloxone also resulted in a reduction in resting core temperature (TC) in the light but not the dark phase. It did not affect the weight loss or hypothermia which accompanied 24 h food and water deprivation. Naloxone did, however, suppress FI and WI following deprivation and inhibited the recovery of body weight thereafter. The influence of naloxone upon FI, WI, TC and body weight was dose-dependent over 0.05–0.50 mg/kg/h. Increasing the dose to 3.0 mg/kg/h eliminated the anticiceptive action of U50, 488H revealing a blockade of κ- (in addition to μ-) receptors. This higher dose was not more effective in reducing FI, WI, body weight and TC than 0.5 mg/kg/h. Further, treatment with MR 2266, an antagonist (or weak partial agonist) with a higher activity at κ-receptors than naloxone, was not more effective than naloxone in reducing FI, WI and body weight: further, it did not affect TC. Moreover, chronic infusion of bremazocine, (a κ-agonist and μ-antagonist) reduced WI, FI, body weight and TC by a magnitude comparable to that of naloxone. Finally, chronic infusion of the μ-agonist, sufetanyl, led to a sustained rise in TC. It is concluded, that: (1) μ-opioid receptors may play a major role in the modulation of daily FI and WI and of body weight in freely behaving rats: this action in expressed in both the light and dark phases of the cycle and maintained following deprivation. The data provide no evidence for (but do not exclude) a particular role of κ-receptors. (2) μ-Receptors play a physiological role in the modulation of TC in the light but not the dark phase of the daily cycle.     

Effect of systemic and intrathecal gabapentin on allodynia in a new rat model of postherpetic neuralgia

Patients with postherpetic neuralgia often have an increased sensitivity to a tactile stimulus but impaired thermal sensitivity in the same affected dermatomes. We recently found that depletion of capsaicin-sensitive afferents by systemic treatment with a potent TRPV1 agonist, resiniferotoxin, in adult rats produces long-lasting paradoxical changes in mechanical and thermal sensitivities, which resemble the unique clinical features of postherpetic neuralgia. The anticonvulsant gabapentin is effective in reducing the subjective pain score in patients with postherpetic neuralgia. In this study, we quantified the potential effect of systemic and intrathecal gabapentin on tactile allodynia induced by resiniferotoxin in rats. Intraperitoneal injection of 200 microg/kg resiniferotoxin produced a rapid and sustained increase in the paw withdrawal latency to a radiant heat stimulus. Profound tactile allodynia developed in all the resiniferotoxin-treated rats within 3 weeks. Intraperitoneal injection of 30-60 mg/kg of gabapentin in resiniferotoxin-treated rats significantly increased the withdrawal threshold in response to von Frey filaments. Furthermore, intrathecal administration of 10-30 microg of gabapentin also produced a significant effect on the mechanical withdrawal threshold in all resiniferotoxin-treated rats. These data provide complementary new information that gabapentin administered systemically and spinally can effectively relieve tactile allodynia in this animal model of postherpetic neuralgia.     

The time course of intracranial pathophysiological changes following experimental subarachnoid haemorrhage in the rat

The rat subarachnoid haemorrhage (SAH) model was further studied to establish the precise time course of the globally reduced CBF that follows and to ascertain whether temporally related changes in cerebral perfusion pressure (CPP) and intracranial pressure (ICP) take place. Parallel ultrastructural studies were performed upon cerebral arteries and their adjacent perivascular subarachnoid spaces. SAH was induced by a single intracisternal injection of autologous arterial blood. Serial measurements of regional cortical CBF by hydrogen clearance revealed that experimental SAH resulted in an immediate 50% global reduction in cortical flows that persisted for up to 3 h post SAH. At 24 h, flows were still significantly reduced at 85% of control values (p less than 0.05), but by 48 h had regained normal values and were maintained up to 5 days post SAH. ICP rose acutely after haemorrhage to nearly 50 mm Hg with C-type pressure waves being present. ICP then fell slowly, only fully returning to control levels at 72 h. Acute hydrocephalus was observed on autopsy examination of SAH animals but not in controls. Reductions in CPP occurred post SAH, but only in the order of 15%, which could not alone account for the fall in CBF that took place. At 48 and, to a lesser extent, 24 h post SAH, myonecrosis confined largely to smooth muscle cells of the immediately subintimal media was observed. No significant changes in the intima or perivascular nerve plexus were seen. Within 24 h of haemorrhage, a limited degree of phagocytosis of erythrocytes by pial lining cells took place. However, early on the second day post SAH, a dramatic increase in the numbers of subarachnoid macrophages arose from a transformation of cells of the pia-arachnoid. This period was characterised by intense phagocytic activity, erythrocytes, fibrin, and other debris being largely cleared over the next 24 h. At 5 days post SAH the subarachnoid macrophage population declined, cells losing their mobile active features to assume a more typical pia-arachnoid cell appearance once more. Our studies indicate that this increasingly utilised small animal model of SAH develops global cortical flow changes only acutely, and it is likely that early vasospasm, secondary to released blood products rather than pressure changes per se, is responsible for the initial cerebral ischaemia that develops. Interestingly, both cerebral arterial vasculopathy and perivascular macrophage phagocytic activity are most marked at approximately 48 h following SAH in the rat, a time at which a phase of delayed cerebral arterial narrowing has previously been documented.     

Regional changes of tissue pH and ATP content in rat brain following systemic administration of kainic acid

Regional metabolic alterations induced by systemic administration of kainic acid were investigated in rat brains. The histochemical study revealed that an acidic pH shift preceded an ATP decrease in the limbic structures. In the hippocampal Ammon's horn, it was noted that a selective decrease of ATP occurred in the dendritic subfield, such as the stratum radiatum and/or the stratum oriens. It was suggested that this selective ATP decrease in the dendrite is directly related to kainate neurotoxicity.     

The effects of interleukin-1 beta on the activity of adrenal, splenic and renal sympathetic nerves in the rat.

The effects of intravenous (i.v.) administration of recombinant human interleukin-1 beta (rhIL-1 beta) on the activity of adrenal, splenic and renal sympathetic nerves were observed in urethane-anesthetized rats. An i.v. injection of IL-1 beta in doses of 10 pg-20 ng per animal (300-400 g, b.w.) resulted in a dose-dependent increase in the activity of the adrenal and splenic nerves, which lasted for more than 2-6 h. On the other hand, the activity of renal nerves showed a transient increase which was followed by a long-lasting suppression after injection of rhIL-1 beta (100 pg, i.v.). An i.v. injection of cyclooxygenase inhibitors (6 mg ibuprofen or 20 mg sodium salicylate) suppressed almost completely the rhIL-1 beta (100 pg)-induced activity in adrenal and splenic nerves. Although rhIL-1 beta (100 pg, i.v.) produced a fall in arterial blood pressure, baroreceptor denervation did not affect the excitatory responses of the adrenal and splenic nerves to rhIL-1 beta. The results suggest the regional differentiation of activity in the visceral sympathetic nerves in response to rhIL-1 beta. The rhIL-1 beta-induced activation of splenic sympathetic nerves implicates their involvement in the modulation of immunity by brain.     

Long-term time course of regional changes in cholinergic indices following transient ischemia in the spontaneously hypertensive rat brain

Using an animal model of forebrain ischemia in spontaneously hypertensive rats (SHR) by 3-h bilateral carotid occlusion, and various indices of the cerebral cholinergic system were assessed for periods up to 24 weeks. The lesions observed histologically in the hippocampus of SHR 2 weeks after ischemia were less severe than those in the frontal cortex. Marked elevation of acetylcholine concentration was transiently observed in the frontal cortex, hippocampus and thalamus + midbrain at 2 weeks, and in the striatum at 1–4 weeks after ischemia. Choline acetyltransferase activity remained unchanged in all regions throughout the experimental period except for a minimal decrease in the frontal cortex at 4 weeks. Choline esterase (ChE) activity was slightly decreased in the frontal cortex at 2–4 weeks after ischemia but recovered by 8 weeks. A decrease in the hippocampus was seen at 8 weeks. The B_max for the M1-receptor was significantly reduced by 2 weeks in the frontal cortex and by 4 weeks in the hippocampus. Low B_max values in both regions persisted through week 24. These delayed hippocampul changes in the ChE activity and M1-receptor in SHR were similar to those of the very much delayed changes in M1-receptor previously reported in the gerbil model for transient ischemia. In contrast, Wistar-Kyoto rats (WKY), used as normotensive controls, exhibited no histological or biochemical changes for up to 24 weeks. The difference between SHR and WKY may depend on the more severe cerebral blood flow depletion during carotid ligation in the former. The chronic state of SHR after the transient ischemia may be a useful pathophysiological model for human cerebral infarctions with hypertension.     

Blockade of supraspinal 5-HT1A receptors potentiates the inhibitory effect of venlafaxine on wind-up activity in mononeuropathic rats

In mononeuropathic rats submitted to a C-fiber reflex responses paradigm, repeated administration (five successive injections every half-life) of 10 mg/kg, s.c. of venlafaxine, but not of 2.5 mg/kg, s.c., a mixed monoamine reuptake inhibitor with preferential inhibitory activity in 5-HT reuptake, induced a progressive reduction of spinal wind-up. Repeated co-administration of the selective 5-HT1A receptor antagonist WAY 100,635 i.c.v. (50 microg/injection) significantly increased the effect of venlafaxine s.c., indicating that venlafaxine-induced inhibition of spinal wind-up in mononeuropathic rats is potentiated by blockade of central 5-HT1A receptors.     

Remote long-term registrations of sleep-wake rhythms, core body temperature and activity in marmoset monkeys

Initial studies in the day active marmoset monkey (Callithrix jacchus) indicate that the sleep-wake cycle of these non-human primates resembles that of humans and therefore conceivably represent an appropriate model for human sleep. The methods currently employed for sleep studies in marmosets are limited. The objective of this study was to employ and validate the use of specific remote monitoring system technologies that enable accurate long-term recordings of sleep-wake rhythms and the closely related rhythms of core body temperature (CBT) and locomotor activity in unrestrained group-housed marmosets. Additionally, a pilot sleep deprivation (SD) study was performed to test the recording systems in an applied experimental setup. Our results show that marmosets typically exhibit a monophasic sleep pattern with cyclical alternations between NREM and REM sleep. CBT displays a pronounced daily rhythm and locomotor activity is primarily restricted to the light phase. SD caused an immediate increase in NREM sleep time and EEG slow-wave activity as well as a delayed REM sleep rebound that did not fully compensate for REM sleep that had been lost during SD. In conclusion, the combination of two innovative technical approaches allows for simultaneous measurements of CBT, sleep cycles and activity in multiple subjects. The employment of these systems represents a significant refinement in terms of animal welfare and will enable many future applications and longitudinal studies of circadian rhythms in marmosets.