scholarly journals A Sub-Minute Resolution Prediction of Brain Temperature Based on Sleep-Wake State in the Mouse

2020 ◽  
Author(s):  
Yaniv Sela ◽  
Marieke M.B. Hoekstra ◽  
Paul Franken
Keyword(s):  
Brain Temperature ◽  
Clinical Importance ◽  
Time Of Day ◽  
Mathematical Tool ◽  
Profound Influence ◽  
Cortical Temperature ◽  
Main Factors ◽  
Similar Accuracy ◽  
Wake State ◽  
Independent Cohort

AbstractWhile brain temperature is of neurobiological and clinical importance, it is still unclear which factors contribute to its daily dynamics and to what degree. We recorded cortical temperature in mice alongside sleep-wake state during 4 days including a 6h sleep deprivation, and developed a mathematical tool to simulate temperature based on the sleep-wake sequence. The model estimated temperature with remarkable precision accounting for 91% of its variance based on three main factors with the sleep-wake sequence accounting for most of the variance (74%) and time-of-day (‘circadian’) the least (9%). As third factor, prior wake prevalence, was discovered to up-regulate temperature, explaining 43% of the variance. With similar accuracy the model predicted cortical temperature in a second, independent cohort using the parameters optimized for the first. Our model corroborates the profound influence of sleep-wake state on brain temperature, and can help differentiate thermoregulatory from sleep-wake driven effects in experiments affecting both.

scholarly journals Sub-minute prediction of brain temperature based on sleep–wake state in the mouse

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Yaniv Sela ◽  
Marieke MB Hoekstra ◽  
Paul Franken
Keyword(s):  
Statistical Approach ◽  
Brain Temperature ◽  
Clinical Importance ◽  
Time Of Day ◽  
Mathematical Tool ◽  
Profound Influence ◽  
Cortical Temperature ◽  
Similar Accuracy ◽  
Wake State ◽  
Independent Cohort

Although brain temperature has neurobiological and clinical importance, it remains unclear which factors contribute to its daily dynamics and to what extent. Using a statistical approach, we previously demonstrated that hourly brain temperature values co-varied strongly with time spent awake (Hoekstra et al., 2019). Here we develop and make available a mathematical tool to simulate and predict cortical temperature in mice based on a 4-s sleep–wake sequence. Our model estimated cortical temperature with remarkable precision and accounted for 91% of the variance based on three factors: sleep–wake sequence, time-of-day (‘circadian’), and a novel ‘prior wake prevalence’ factor, contributing with 74%, 9%, and 43%, respectively (including shared variance). We applied these optimized parameters to an independent cohort of mice and predicted cortical temperature with similar accuracy. This model confirms the profound influence of sleep–wake state on brain temperature, and can be harnessed to differentiate between thermoregulatory and sleep–wake-driven effects in experiments affecting both.

Acclimation, temperature selection, and heat exchange in the turtle, Chrysemys scripta

1980 ◽  
Vol 238 (5) ◽  
pp. R443-R446 ◽  
Author(s):  
L. I. Crawshaw ◽  
M. H. Johnston ◽  
D. E. Lemons
Keyword(s):  
Heart Rate ◽  
Initial Temperature ◽  
Brain Temperature ◽  
Time Of Day ◽  
Acclimation Temperature ◽  
Mean Body Temperature ◽  
Rapid Changes ◽  
Ambient Water Temperature ◽  
The Brain ◽  
Turtle Heart

Turtles acclimated to temperatures between 3 and 19 degrees C were placed in a thermal gradient. The animals usually selected temperatures above 28 degrees C within 1 h after placement in the gradient, attaining a final thermal preferendum between 31 and 33 degrees C. Turtles placed in the gradient for extended periods of time were more active during the day; the temperature selected was not related to activity or time of day. Turtles were transferred from a constant temperature bath at 10 or 30 degrees C to a calorimeter at 30 or 10 degrees C. Mean body temperature (Tb) and temperatures of the heart (The), brain (Tbr), and cloaca (Tcl) as well as heart rate were continuously monitored. In a 0.76-kg turtle, temperatures increased to two-thirds of the final difference between the initial temperature and the final temperature in the following times (min): Tb, 5.5; The, 6.0; Tcl, 9.0. The increase in Tbr varied depending on whether the head was extended or retracted. Rapid changes in ambient water temperature had relatively little effect on the heart rate of a submerged turtle. Heart rates were closely related to The and were practically independent of brain temperature.

Interleukin-1 induces changes in sleep, brain temperature, and serotonergic metabolism

1997 ◽  
Vol 272 (2) ◽  
pp. R601-R606 ◽  
Author(s):  
C. Gemma ◽  
L. Imeri ◽  
M. G. de Simoni ◽  
M. Mancia
Keyword(s):  
Time Course ◽  
Preoptic Area ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Secondary Effect ◽  
Intracerebroventricular Injection ◽  
Early Increase ◽  
Cortical Temperature ◽  
Freely Moving

Simultaneous recordings of sleep-wake activity and of serotonergic metabolism in the medial preoptic area were performed in freely moving rats after the intracerebroventricular injection of interleukin-1 (IL-1) at dark onset. IL-1 (2.5 ng) induced a biphasic increase in slow-wave sleep and an early increase in serotonergic metabolism starting 30 min postinjection. Phasic, state-specific changes (which have been described in spontaneous sleep) were superimposed on this tonic, overall increase in serotonergic metabolism. IL-1 (25 ng) induced an increase in wakefulness and a delayed increase in serotonergic metabolism, which started 120 min postinjection. This suggests that the time course of the serotonergic activation could play a role in mediating IL-1 effects on sleep. Both doses of IL-1 induced a similar and significant increase in brain cortical temperature, suggesting that IL-1 effects on sleep are not a secondary effect of the increase in cortical temperature and that the serotonergic system is not involved in IL-1-induced fever.

Time of day is an inaccurate surrogate marker for sleep-wake state in an epilepsy monitoring unit

2021 ◽  
Vol 169 ◽  
pp. 106524
Author(s):  
Kevin H. Ha ◽  
Andrew C. Schomer ◽  
Juliana Leonardo ◽  
Mark Quigg
Keyword(s):  
Surrogate Marker ◽  
Time Of Day ◽  
Epilepsy Monitoring ◽  
Wake State

scholarly journals Brief anesthesia, but not voluntary locomotion, significantly alters cortical temperature

2015 ◽  
Vol 114 (1) ◽  
pp. 309-322 ◽  
Author(s):  
Michael J. Shirey ◽  
Jared B. Smith ◽  
D'Anne E. Kudlik ◽  
Bing-Xing Huo ◽  
Stephanie E. Greene ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Computational Models ◽  
Brain Temperature ◽  
Core Body Temperature ◽  
Field Potential ◽  
Vessel Diameter ◽  
Two Photon Microscopy ◽  
Convolution Model ◽  
Cortical Temperature ◽  
The Brain

Changes in brain temperature can alter electrical properties of neurons and cause changes in behavior. However, it is not well understood how behaviors, like locomotion, or experimental manipulations, like anesthesia, alter brain temperature. We implanted thermocouples in sensorimotor cortex of mice to understand how cortical temperature was affected by locomotion, as well as by brief and prolonged anesthesia. Voluntary locomotion induced small (∼0.1°C) but reliable increases in cortical temperature that could be described using a linear convolution model. In contrast, brief (90-s) exposure to isoflurane anesthesia depressed cortical temperature by ∼2°C, which lasted for up to 30 min after the cessation of anesthesia. Cortical temperature decreases were not accompanied by a concomitant decrease in the γ-band local field potential power, multiunit firing rate, or locomotion behavior, which all returned to baseline within a few minutes after the cessation of anesthesia. In anesthetized animals where core body temperature was kept constant, cortical temperature was still >1°C lower than in the awake animal. Thermocouples implanted in the subcortex showed similar temperature changes under anesthesia, suggesting these responses occur throughout the brain. Two-photon microscopy of individual blood vessel dynamics following brief isoflurane exposure revealed a large increase in vessel diameter that ceased before the brain temperature significantly decreased, indicating cerebral heat loss was not due to increased cerebral blood vessel dilation. These data should be considered in experimental designs recording in anesthetized preparations, computational models relating temperature and neural activity, and awake-behaving methods that require brief anesthesia before experimental procedures.

Effects of systemic GHRH on sleep in intact and hypophysectomized rats

1996 ◽  
Vol 270 (2) ◽  
pp. E230-E237 ◽  
Author(s):  
F. Obal ◽  
R. Floyd ◽  
L. Kapas ◽  
B. Bodosi ◽  
J. M. Krueger
Keyword(s):  
Human Subjects ◽  
Physiological Saline ◽  
Time Of Day ◽  
Light Onset ◽  
Gh Secretion ◽  
Pituitary Growth Hormone ◽  
Hypophysectomized Rats ◽  
Cortical Temperature ◽  
Intact Rats

The role of pituitary growth hormone (GH) in the mediation of enhanced sleep elicited by GH-releasing hormone (GHRH) was studied in the rat. Intact and hypophysectomized (HYPOX) rats received systemic injections of GHRH or physiological saline. GHRH (0.5, 5.0, or 50 micrograms/kg in the intact rats and 0.5 or 50 micrograms/kg in HYPOX rats) was injected 6 h after light onset (P.M. injection) or just before light onset (A.M. injection, 0.5 microgram/kg in both A.M. groups). Sleep-wake activity and brain cortical temperature were recorded for 23 h (12 h light + 11 h dark). A.M. injection of GHRH did not alter sleep in normal or HYPOX rats. Each dose of P.M. GHRH increased rapid-eye-movement sleep (REMS) during 6 h postinjection in the intact rats. Hypophysectomy abolished the REMS-promoting activity of GHRH. P.M. injection of 0.5 microgram/kg GHRH increased non-REM sleep (NREMS) and enhanced electroencephalogram slow-wave activity during NREMS in both the intact and the HYPOX rats. The NREMS-promoting activity disappeared when the dose of GHRH was increased in the intact rats, whereas a tendency to enhanced NREMS was still observed after 50 micrograms/kg GHRH in the HYPOX rats. GHRH stimulated GH secretion dose dependently in the intact rats. A.M. injection of 0.5 microgram/kg GHRH tended to be less effective in stimulating GH release than the same dose administered P.M. The results confirm the time-of-day variations in the GHRH effects on sleep previously reported in human subjects. It is likely that pituitary GH is involved in the mediation of the REMS-promoting activity of GHRH but not in the NREMS-promoting activity of GHRH. Nevertheless, the results do not exclude the possibility that GH may modulate NREMS.

Effects of temperature on sleep in the developing rat

1998 ◽  
Vol 274 (4) ◽  
pp. R1087-R1093
Author(s):  
Roger N. Morrissette ◽  
H. Craig Heller
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
State Structure ◽  
Rat Pups ◽  
The Relationship ◽  
Developing Rat ◽  
Wake State

In altricial species, such as humans and rats, much of the development of autonomic systems occurs postnatally. Consequently, vulnerabilities exist early in postnatal development when immature autonomic functions are challenged by external factors such as variations in ambient temperature (Ta). Ta profoundly influences sleep/wake state structure in adult animals and humans, and exposure to excessive warmth has been implicated as a risk factor in sudden infant death syndrome. To better understand the relationship between temperature and sleep during development, we investigated the effect of Ta variation on sleep/wake state structure and sleep intensity in developing rats. In this experiment, sleep intensity was measured by the intensity of slow-wave activity during slow-wave sleep. Neonatal Long-Evans hooded rat pups were surgically prepared for chronic sleep/wake state and brain temperature (Tbr) recording. Two-hour recordings of sleep/wake state and Tbr were obtained from rats on postnatal day 12( P12), P14, P16, P18, and P20 at a Ta of either 28.0–30.0, 33.0–35.0, or 38.0–40.0°C. Ta significantly influenced sleep/wake state structure but had little, if any, effect on sleep intensity in developing rats.

scholarly journals Muramyl dipeptide and IL-1 effects on sleep and brain temperature after inhibition of serotonin synthesis

1997 ◽  
Vol 273 (5) ◽  
pp. R1663-R1668 ◽  
Author(s):  
Luca Imeri ◽  
Susanna Bianchi ◽  
Mauro Mancia
Keyword(s):  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Muramyl Dipeptide ◽  
Serotonin Synthesis ◽  
System 2 ◽  
Cortical Temperature ◽  
Second Phases ◽  
Freely Moving

The role of the interactions between serotonin (5-HT) and muramyl dipeptide (MDP) and interleukin-1 (IL-1) in sleep control and thermoregulation was evaluated. To this purpose, MDP and IL-1 were injected intracerebroventricularly at dark onset into freely moving rats pretreated twice intraperitoneally with para-chlorophenylalanine (PCPA) (300 mg/kg), which depletes brain 5-HT and causes insomnia. Fever and slow-wave sleep (SWS) enhancement induced by 150 pmol MDP were completely blocked in PCPA-pretreated rats. Only the first phase of the biphasic increase in SWS induced by 2.5 ng IL-1 was suppressed by PCPA pretreatment, whereas fever remained unaffected. These results suggest that 1) MDP effects on both sleep-wake activity and brain cortical temperature are mediated by the serotonergic system; 2) the mechanisms mediating the first and the second phases of IL-1-induced SWS excess are different: 5-HT could be involved in the first phase, but not in the second one; and 3) the 5-HT system does not appear to be involved in IL-1-induced fever.

scholarly journals Diurnal brain temperature rhythms and mortality after brain injury: a prospective and retrospective cohort study

2021 ◽  
Author(s):  
Nina M Rzechorzek ◽  
Michael J Thrippleton ◽  
Francesca M Chappell ◽  
Grant Mair ◽  
Ari Ercole ◽  
...  
Keyword(s):  
Intensive Care ◽  
Brain Temperature ◽  
Brain Regions ◽  
Time Of Day ◽  
Clinical Settings ◽  
List Type ◽  
Brain Injured ◽  
Injured Patients ◽  
Healthy Participants ◽  
Deep Brain

ABSTRACTObjectiveTo determine the clinical relevance of brain temperature (TBr) variation in patients after traumatic brain injury (TBI).DesignCohort study with prospective (healthy participant) and retrospective (TBI patient) arms.SettingSingle neuroimaging site in the UK (prospective arm); intensive care sites contributing to the Collaborative European NeuroTrauma Effectiveness Research in TBI (CENTER-TBI) High Resolution ICU (HR ICU) Sub-Study (retrospective arm).Participants40 healthy adults aged 20-40 years recruited for non-invasive brain thermometry and all patients up to May 2020 that had TBr measured directly and were not subjected to Targeted Temperature Management (TTM).Main outcome measuresA diurnal change in TBr (healthy participants); death in intensive care (patients).ResultsIn healthy participants, mean TBr (38.5 SD 0.4°C) was higher than oral temperature (36.0 SD 0.5°C), and 0.36°C higher in luteal females relative to follicular females and males (95% confidence interval 0.17 to 0.55, P=0.0006 and 0.23 to 0.49, P<0.0001, respectively). TBr increased with age, most notably in deep brain regions (0.6°C over 20 years; 0.11 to 1.07, P=0.0002). The mean maximal spatial TBr range was 2.41 (SD 0.46)°C, with highest temperatures in the thalamus. TBr varied significantly by time of day, especially in deep brain regions (0.86°C; 0.37 to 1.26, P=0.0001), and was lowest in the late evening. Diurnal TBr in cortical white matter across participants ranged from 37.0 to 40.3°C. In TBI patients (n=114), mean TBr (38.5 SD 0.8°C) was significantly higher than body temperature (TBo 37.5 SD 0.5°C; P<0.0001) and ranged from 32.6 to 42.3°C. Only 25/110 patients displayed a diurnal temperature rhythm; TBr amplitude was reduced in older patients (P=0.018), and 25/113 patients died in intensive care. Lack of a daily TBr rhythm, or an age increase of 10 years, increased the odds of death 12-fold and 11-fold, respectively (OR for death with rhythm 0.09; 0.01 to 0.84, P=0.035 and for death with ageing by 1 year 1.10; 1.05 to 1.16, P=0.0002). Mean TBr was positively associated with survival (OR for death 0.45 for 1°C increase; 0.21 to 0.96, P=0.040).ConclusionsHealthy TBr exceeds TBo and varies by sex, age, menstrual cycle, brain region, and time of day. Our 4-dimensional reference resource for healthy TBr can guide interpretation of TBr data in multiple clinical settings. Daily temperature variation is frequently disrupted or absent in TBI patients, in which TBr variation is of greater prognostic use than absolute TBr. Older TBI patients lacking a daily TBr rhythm are at greatest risk of death in intensive care. Appropriately controlled trials are needed to confirm the predictive power of TBr rhythmicity in relation to patient outcome, as well as the clinical utility of TTM protocols in brain-injured patients.RegistrationUK CRN NIHR CPMS 42644; ClinicalTrials.gov number, NCT02210221.SUMMARY BOXWhat is already known on this topicBrain temperature (TBr) can be measured directly in brain-injured patients via intracranial probe, but this method cannot be used in healthy individuals.TBr can be measured non-invasively using magnetic resonance spectroscopy (MRS), but this method is not appropriate for most brain-injured patients.Since physiological reference ranges for TBr in health have not been established, the clinical relevance of TBr variation in patients is unknown, and the use of TTM in neurocritical care remains controversial.What this study addsA reference map for healthy adult TBr at three clinically-relevant time points that can guide interpretation of TBr measured directly, or by MRS, in multiple clinical settings.Our results suggest that loss of diurnal TBr rhythmicity after TBI increases the odds of intensive care death 12-fold; some TTM strategies may be clinically inappropriate.

scholarly journals Spread?F and the Perturbations of the Maximum Electron Density of the F Layer

1962 ◽  
Vol 15 (2) ◽  
pp. 242 ◽  
Author(s):  
DG Singleton
Keyword(s):  
Electron Density ◽  
Critical Frequency ◽  
Magnetic Activity ◽  
Time Of Day ◽  
Dominant Effect ◽  
Middle Latitudes ◽  
Profound Influence ◽  
Maximum Electron Density ◽  
Spread F ◽  
Range Of Values

An analysis has been made of spread-F data obtained from LG.Y. f-plots for several ionosonde stations grouped about longitude 75� W. to establish whether there is any connection between the severity of frequency-spreading (ilJ) and the time of day, season of the year, magnetic activity, height of the F layer, critical frequency of the F layer, and the latitude of the ionosonde station. The diurnal variations of the severity of frequency spreading are found to vary considerably with latitude and season and no clear pattern emerges. Magnetic activity affects the value of ilf but again in a complex way which varies with latitude. The magnitude of ilf seems to be greatest when the layer is high and descending at low and middle latitudes but not at high latitudes. At all latitudes the magnitude of ilf is greatest when the critical frequency is lowest. This is considered to be the dominant effect having a profound influence on the diurnal and seasonal distributions of ilf. These results are discussed in terms of the hypothesis that frequency spreading is due to the availability of a range of values of N IDJ1x. at the maximum of the F2 layer. This range of values is thought to correspond to a system of irregularities each involving an enhancement or a deficiency of electron density relative to the background ionization. The extra ionization involved in the irregularities is estimated to be of the order of 10' electrons/c.c. and is found to vary little with season, magnetic activity, and latitude.

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