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Electroencephalographic methods were used to study effects of preparation of the exogenous heat shock protein with molecular mass of 70 kDa (Hsp70i/Hsc70) on time characteristics of sleep and wakefulness, brain temperature, peripheral vasomotor reactions, and thoracic muscle contractile activity after the 5-hour forceful sleep deprivation in the pigeon Columba livia. Administration of Hsp70i/Hsc70 into the third brain ventricle at once after the end of sleep deprivation eliminated disturbances in the sleep-wakefulness cycle organization and decreased the thoracic muscle contractile activity and the brain temperature as early as for the first hour of postdeprivation period. For the subsequent hours, the Hsp70i/Hsc70 action was characterized by an increase of the total time of deep sleep and a decrease of the total time of the rapid eye movement sleep. We suggest that the protective effects of the exogenous Hsp70i/Hsc70 preparation are associated with its ability to decrease activity of the hypothalamo-pituitary-adrenal axis and to enhance the stress-limiting function of the slow eye movement sleep. [ABSTRACT FROM AUTHOR]

Zajonc and Markus published a chapter in 1984 that proposed solutions to the difficult problem of modeling interactions between cognition and emotion. The most radical of their proposals was the importance of the motor system in information processing. These initial preoccupations, when wedded with the vascular theory of emotional efference (VTEE), propelled theory and research about how the face works to control emotion and to control interpersonal interaction. We discuss the development of Bob’s thinking about facial expression—facial efference is the term he preferred—as he moved toward predictions that sounded radical at the time, and which these days sound like precursors to advances in neuroscience and psychology subsumed under the term “embodied cognition.” [ABSTRACT FROM PUBLISHER]

Abstract: A number of drugs and psychological stressors induce brain hyperthermia and increase extracellular dopamine in the caudate-putamen. The present study tested whether caudate-putamen hyperthermia produced by such stimuli is dependent on dopaminergic transmission. Rats were infused with 6-hydroxydopamine unilaterally into the medial forebrain bundle, and after a two-week recovery period, removable thermocouples were used to monitor temperature in the depleted and intact caudate-putamen in freely-moving animals. The indirect dopamine agonist d-amphetamine (1 and 2mg/kg s.c.) increased caudate-putamen temperature, whereas a low dose of the direct agonist apomorphine (0.1mg/kg s.c.) reduced it. Gamma-butyrolactone, which strongly inhibits dopamine release at the dose administered (700mg/kg i.p.), initially reduced and then increased caudate-putamen temperature. Brief (5-10min) presentation of mild stressors, including tail pinch, produced a rapid and transient caudate-putamen hyperthermia. Quantitative 125I-RTI-55 autoradiography in post-mortem tissue revealed a 97-100% loss of binding to dopamine transporters in the lesioned caudate-putamen. Despite this near-total dopamine denervation, neither basal caudate-putamen temperature, nor any of the observed temperature responses to drugs or mild stressors, was altered. We conclude that in the caudate-putamen, endogenous dopamine is unlikely to modulate temperature significantly at a local level. [Copyright &y& Elsevier]

Automatic control systems of brain temperature for water surface-cooling were first-ever applied to the brain hypothermic treatment of patients. A patient in ICU was regarded as a unity controlled system with an input (temperature of water into blanket) and an output (tympanic membrane temperature). The proposed algorithm of optimal-adaptive and fuzzy control laws inclusive of our developed cooling and warming machine were well confirmed during the hypothermic course to keep brain temperature of patients within its allowable range. It was well controlled without much influence due to room temperature, metabolic and circulatory change caused by various medical treatments including the effect of nonlinear and time-varying characteristics of individual patients. The clinical control of brain temperature was almost continuously performed in around 10 days, under the brain temperature between 35°C and 37°C scheduled by physicians according to the state of patients. Their state had been monitored during the therapeutic course of pharmacological treatment with almost everyday examinations by CT imaging, referring various vital signs inclusive of the temperature of urinary bladder with continuous measurement of intracranial pressure by a catheter placement in cerebral sinus. The patients had good recovery to their rehabilitation after mild hypothermia by the proposed automatic control systems. [ABSTRACT FROM AUTHOR]

Electroencephalographic methods were used to study the effects of total sleep deprivation on thermoregulatory measures of the fever response in pigeons (Columba livia): brain temperature, peripheral vasomotor reactions, thoracic muscle contractile activity, and the recovery of somatic functions and the time characteristics of waking and sleep in lipopolysaccharide (LPS)-induced endotoxemia. Sleep deprivation during the period in which the quantity of slow-wave sleep increased on administration of LPS induced decreases in the latent period of fever onset and in the duration of fever, along with more significant increases in brain temperature and the level of muscle contractile activity as compared with the effects of LPS alone. The period after sleep deprivation was characterized by more prolonged recovery of muscle contractile activity and the time characteristics of sleep and waking states, along with more prolonged compensatory "rebound" of slow-wave sleep as compared with the effects of sleep deprivation alone. Thus, sleep deprivation in endotoxemia led to decreases in the latent period of fever onset, exacerbation of fever, and increases in the latent period of recovery of physiological functions. [ABSTRACT FROM AUTHOR]

Abstract: Since brain metabolism is accompanied by heat production, measurement of brain temperature offers a method for assessing global alterations in metabolic neural activity. This approach, high-resolution (5-s bin) temperature recording from the nucleus accumbens (NAcc), temporal muscle, and facial skin, was used to study motivated drinking behavior in rats. Experienced animals were presented with a cup containing 5-ml of Coca-Cola® (Coke) beverage that resulted, within certain latencies, in initiation of a continuous chain of licking until all liquid was fully consumed. While cup presentation induced rapid, gradual NAcc temperature increase peaking at the start of drinking, temperatures slowly decreased during Coke consumption, but phasically increased again in the post-consumption period when rats were hyperactive, showing multiple interactions with an empty cup. Muscle temperatures followed a similar pattern, but the changes were weaker and delayed compared to those in the brain. Skin temperature rapidly dropped after cup presentation, steadily maintained at low levels during consumption, and slowly restored during the post-consumption period. Substitution of the expected Coke with either sugar-free Diet Coke® or water resulted in numerous drinking attempts but ultimately no consumption. During these tests, locomotor activation was much greater and more prolonged, brain and muscle temperatures increased monophasically, and their elevation was significantly greater than that with regular Coke tests. Food deprivation decreased drinking latencies, did not change the pattern of temperature fluctuations during Coke consumption, but temperature elevations were greater than in controls. Our data suggest sustained neural activation triggered by appetitive stimuli and associated with activational (seeking) aspects of appetitive motivated behavior. This seeking-related activation is rapidly ceased following consumption, suggesting this change as a neural correlate of reward. In contrast, inability to obtain an expected reward maintains neural activation and seeking behavior, resulting in larger deviations in physiological parameters. [Copyright &y& Elsevier]

Surface cooling by an automatic control system using a water blanket ensures a bloodless method of accurate brain hypothermia for cerebral protection at various stages of medical treatment. The control of temperature without any effects from the outside environment means that medical staff have less need to use their special skills for the exact management of brain temperature in clinical application, although the method is based on an easily handled surface water-cooling system. However, water is not always an appropriate medium for clinical cooling, from the viewpoint of both patients and the medical staff, because of the maintenance of the system in an intensive care unit (ICU). In order to cope with such difficulties, air-cooling is proposed based on various simulation results. Here, the aim is to realize automatic temperature control based on a fuzzy algorithm as a clinical reflection of the medical staff’s knowledge and experience. Experiments were carried out using a mannequin with human thermal characteristics in order to verify the utility of the basic automatic air-cooling control system for the treatment of brain hypothermia. [ABSTRACT FROM AUTHOR]

Abstract: The present study examined the physiological mechanisms of the responses of brain tissue oxygen partial pressure (PtO2), brain temperature (T brain), global oxygen consumption (V̇O2), and respiratory frequency (f R) to hypoxia in non-sedated and non-anesthetized arctic ground squirrels (Spermophilus parryii, AGS) and rats. We found that (1) in contrast to oxygen partial pressure in blood (PaO2), the baseline value of PtO2 in summer euthermic AGS is significantly higher than in rats; (2) both PtO2 and PaO2 are dramatically reduced by inspired 8% O2 in AGS and rats, but AGS have a greater capacity in PtO2 to cope with environmental hypoxia; (3) metabolic rate before, during, and after hypoxic exposure is consistently lower in AGS than in rats; (4) the respiratory responding patterns to hypoxia in the two species differ in that f R decreases in AGS but increases in rats. These results suggest that (1) AGS have special mechanisms to maintain higher PtO2 and lower PaO2, and these levels in AGS represent a typical pattern of adaptation of heterothermic species to and a brain protection from hypoxia; (2) AGS brain responds to hypoxia through greater decreases in PtO2 and decreased f R and ventilation. In contrast, rat brain responds to hypoxia by less reduction in PtO2 and increased f R and ventilation. [Copyright &y& Elsevier]

Direct measurements of deep-brain and body-core temperature were performed on rats to determine the influence of cerebral blood flow (CBF) on brain temperature regulation under static and dynamic conditions. Static changes of CBF were achieved using different anesthetics (chloral hydrate, CH; α-chloralose, αCS; and isoflurane, IF) with αCS causing larger decreases in CBF than CH and IF; dynamic changes were achieved by inducing transient hypercapnia (5% CO2 in 40% O2 and 55% N2). Initial deep-brain/body-core temperature differentials were anesthetic-type dependent with the largest differential observed with rats under αCS anesthesia (ca. 2°C). Hypercapnia induction raised rat brain temperature under all three anesthesia regimes, but by different anesthetic-dependent amounts correlated with the initial differentials—αCS anesthesia resulted in the largest brain temperature increase (0.32 ± 0.08°C), while CH and IF anesthesia lead to smaller increases (0.12 ± 0.03 and 0.16 ± 0.05°C, respectively). The characteristic temperature transition time for the hypercapnia-induced temperature increase was 2–3 min under CH and IF anesthesia and ~4 min under αCS anesthesia. We conclude that both, the deep-brain/body-core temperature differential and the characteristic temperature transition time correlate with CBF: a lower CBF promotes higher deep-brain/body-core temperature differentials and, upon hypercapnia challenge, longer characteristic transition times to increased temperatures. [ABSTRACT FROM AUTHOR]

Marsupials reportedly can implement selective brain cooling despite lacking a carotid rete. We measured brain (hypothalamic) and carotid arterial blood temperatures every 5 min for 5, 17, and 63 days in spring in three free-living western grey kangaroos. Body temperature was highest during the night, and decreased rapidly early in the morning, reaching a nadir at 10:00. The highest body temperatures recorded occurred sporadically in the afternoon, presumably associated with exercise. Hypothalamic temperature consistently exceeded arterial blood temperature, by an average 0.3°C, except during these afternoon events when hypothalamic temperature lagged behind, and was occasionally lower than, the simultaneous arterial blood temperature. The reversal in temperatures resulted from the thermal inertia of the brain; changes in the brain to arterial blood temperature difference were related to the rate of change of arterial blood temperature on both heating and cooling ( P < 0.001 for all three kangaroos). We conclude that these data are not evidence for active selective brain cooling in kangaroos. The effect of thermal inertia on brain temperature is larger than might be expected in the grey kangaroo, a discrepancy that we speculate derives from the unique vascular anatomy of the marsupial brain. [ABSTRACT FROM AUTHOR]

Temperature has a major effect on survival in all animal species. Despite wide variations in climate, organ temperature is regulated 'tightly' by homeostatic mechanisms controlling heat production and conservation, as well as heat loss. Although less is known about the temperature of the healthy or injured human brain, mammalian brain homeothermy involves interplay between neural metabolic heat production, cerebral blood flow and the temperature of incoming arterial blood. Recent advances in invasive and non-invasive thermometry have allowed measurement of brain temperature to be made in man. In health, small differences only exist between local brain and body core temperature. Large (negative) brain-body temperature dissociation, observed in some patients after severe brain damage, does not appear to be a feature of cerebral homeothermy in healthy people. The extent to which changes in brain temperature reflect, or 'drive', secondary cerebral pathology remains uncertain in patients with traumatic brain injury (TBI). Raised temperature may be due to a regulated readjustment in the hypothalamic 'set-point' in response to inflammation and infection, or it may occur as a consequence of damage to the hypothalamus and/or its pathways. Diagnosis of the mechanism of raised temperature; fever v. neurogenic hyperthermia (regulated v. unregulated temperature rise) is difficult to make clinically. Whatever the cause, a 1-2°C rise in brain or body temperature, especially when it develops early after injury, is widely regarded as harmful. There is no clear evidence that fever per se leads directly to worsened neurological damage or poor outcome, nor evidence that antipyretic treatments (pharmacological or cold-induced therapies) preserve damaged brain tissue or result in a better outcome. Part 2 follows part one with a detailed analysis of the evidence for the significance of raised temperature on outcome after TBI. [ABSTRACT FROM AUTHOR]

Abstract: Background:: Accumulating data suggest that schizophrenia patients'' mental status might be modulated by their core/brain temperature. Hence, we intended to assess in vivo brain temperature (T b) of schizophrenia patients vs. healthy subjects and to evaluate its potential association with patients'' mental status. Methods:: Absolute values of T b were measured in 9 neuroleptic-treated schizophrenia patients and 10 healthy comparison subjects using 1H magnetic resonance spectroscopy (MRS). Values were extracted by measuring the chemical shift between the peaks of water and N-acetyl-aspartate in the 1H MRS spectra. Results:: A substantial (about 1.1 °C) and significantly higher occipital–frontal temperature-gradient was found in the schizophrenia patients compared to the healthy controls (1.27 °C vs. 0.18 °C; p =0.032). Furthermore, a trend was found between the above mentioned occipital–frontal temperature-gradient in the schizophrenia patients and the severity of their psychopathology, as assessed by the total Positive and Negative Syndrome Scale (PANSS) scores (r =0.61; p =0.08). Conclusions:: Our findings corroborate previous results indicating putative correlation between core/brain temperature and the mental status of schizophrenia patients, emphasizing the possible role of within patients decreased frontal temperature and a significant occipital–frontal temperature-gradient as modulators of psychopathology. In addition, the MRS technique used for brain temperature assessment seems to be a potential non-invasive method to assess in vivo absolute T b in schizophrenia. [Copyright &y& Elsevier]

Abstract: Mild to moderate differences in brain temperature are known to greatly affect the outcome of cerebral ischemia. The impact of brain temperature on ischemic disorders has been mainly evaluated through pathological analysis. However, no comprehensive analyses have been conducted at the gene expression level. Using a high-density oligonucleotide microarray, we screened 24000 genes in the hippocampus under hypothermic (32 °C), normothermic (37 °C), and hyperthermic (39 °C) conditions in a rat ischemia-reperfusion model. When the ischemic group at each intra-ischemic brain temperature was compared to a sham-operated control group, genes whose expression levels changed more than three-fold with statistical significance could be detected. In our screening condition, thirty-three genes (some of them novel) were obtained after screening, and extensive functional surveys and literature reviews were subsequently performed. In the hypothermic condition, many neuroprotective factor genes were obtained, whereas cell death- and cell damage-associated genes were detected as the brain temperature increased. At all intra-ischemic brain temperatures, multiple molecular chaperone genes were obtained. The finding that intra-ischemic brain temperature affects the expression level of many genes related to neuroprotection or neurotoxicity coincides with the different pathological outcomes at different brain temperatures, demonstrating the utility of the genetic approach. [Copyright &y& Elsevier]

Summary: Aim of the study: Mild therapeutic hypothermia is a promising new therapy for patients resuscitated from cardiac arrest. Early and fast induction of hypothermia seems to be crucial for best results. The aim of the study was to investigate the feasibility and safety of a new surface cooling method using cold metal plates. Subjects and methods: Twelve adult human-sized swine (79±9kg) were cooled from 38 to 33°C brain temperature. The skin surface was covered with −20°C metal plates (M), as compared to ice packs, alcohol rubs, and fans used in a control group (C). Each method was tested during spontaneous circulation and, after re-warming, during cardiac arrest. Temperatures were recorded continuously. Data are given as mean±standard deviation or as median (interquartile range), if not normally distributed. Comparisons between the treatment groups were performed with the independent samples t-test, or the Mann–Whitney rank-sum test. Results: During spontaneous circulation, cooling rates were 9.3±1.4°C/h (M), and 6.1±1.4°C/h (C) (p =0.003); no skin lesions were observed. During cardiac arrest, cooling rates were 4.1°C/h (1.8–4.8) (M), and 3.7°C/h (3.1–5.3) (C) (p =0.9); no skin lesions were observed. Conclusion: Cooling with cold metal plates was an effective method for rapid induction of mild therapeutic hypothermia in adult human-sized swine during spontaneous circulation, without any signs of skin damage. This new surface-cooling device, independent of energy supply during use, should be further investigated. [Copyright &y& Elsevier]

Abstract: The aim of this study was to explore the effects of barbiturate coma on cerebral tissue oxygen tension and cerebrovascular pressure reactivity (PRx), as an index of cerebral autoregulation in severe head injury patients. This was a prospective observational clinical study of 12 patients with severe traumatic brain injury, carried out at a tertiary-level neurosurgical intensive care unit between April 2002 and May 2005. All patients received standard neurosurgical intensive care and monitoring. Probes for intracranial pressure (ICP), brain temperature (BT) and brain tissue oxygenation (PTiO2) were inserted into (noncontused) normal-looking white matter. Cerebrovascular PRx was measured as a moving correlation between ICP and arterial blood pressure. Barbiturate coma was instituted when ICP became refractory (ICP>20 mmHg). All data from the multimodal monitoring were digitally extracted and statistically analysed. The mean ICP decreased with barbiturate coma in eight of the 12 patients (75% of the patients), but only four achieved a value below 20 mmHg. Of eight patients with prebarbiturate PTiO2 levels above 10 mmHg, six had a further improvement in oxygenation. Thus, concordant favourable changes in ICP, PRx and PTiO2 with barbiturate coma were seen in those who survived. Effective response to barbiturates can be detected by improved PTiO2 and autoregulation (PRx) in severe head injury patients. [Copyright &y& Elsevier]

Abstract: Delayed neurological deficit occurs among 30% of patients after aneurysmal subarachnoid haemorrhage, mainly related to cerebral vasospasm. The early detection of cerebral ischemia remains problematic. Conventional cerebral monitoring (as intracranial pressure and cerebral perfusion pressure) appears to be insufficient, because cerebral ischemia may occur without elevated intracranial pressure. Global cerebral monitoring as venous jugular oxygen saturation are useful for regional monitoring. Local monitoring as oxygen tissue partial pressure (PtiO2) and microdialysis are sensible for brain ischemia detection, but may also ignore episodes occurring in non-monitored brain area. For the detection of most episodes of brain ischemia, several monitoring system should be use performing a multimodal intracerebral monitoring. Brain microdialysis and oxygen tissue partial pressure are promising monitoring system. [Copyright &y& Elsevier]

Background: The purpose of the present experimental study was to determine the feasibility and usefulness of brain temperature measurement (Tbr) and the calculated difference between brain temperature and arterial blood temperature (ΔTbr-a) in uninjured brain during variations of cerebral perfusion pressure (CPP) and concomitant changes of the regional cerebral blood flow (rCBF). Methods: Nine anaesthetized pigs were subjected to controlled CPP decrease to assess the lower cerebral autoregulation threshold. A parenchymal intracranial pressure (ICP) sensor combined with a microthermistor for temperature measurement, a miniaturized Clark-type electrode measuring brain tissue oxygenation (ptiO2), a small flexible intraparenchymal thermodilution probe for measuring rCBF and cerebral microdialysis were inserted carefully in the frontal white matter. Results: Analysing the ptiO2 during controlled CPP decrease, we found significant breakpoints of ptiO2 at a CPP of 40 mmHg and 20 mmHg, related to an rCBF of 20 ml/100 g/min and approximately 10 ml/100 g/min. Similarly, the relationship between ΔTbr-a, and CPP or rCBF revealed a characteristic increase of ΔTbr-a in the negative direction up to more than –0.30 °C assuming a strong flow dependency. Conclusion: The temperature difference between brain tissue and arterial blood ΔTbr-a mainly reflects the cerebral blood flow–brain tissue oxygenation–metabolism relationship as far as the estimation of the individual lower cerebral autoregulation threshold. [ABSTRACT FROM AUTHOR]

The automatic control system for brain tissue temperature is studied theoretically for brain hypothermia treatment. In order to realize a human-friendly control mechanism, an automatic temperature regulation system is constructed to simulate brain hypothermia treatment by introducing a fuzzy algorithm for possible characteristic changes in patients. The brain temperature model is successfully realized to follow the desired temperature course automatically. The model reference fuzzy control of brain temperature based on water-cooling blankets is verified for clinical application to brain hypothermia treatments through various kinds of simulation experiment. [ABSTRACT FROM AUTHOR]

Abstract: Global forebrain ischemia arising from brief occlusion of the carotid arteries in gerbils produces selective hippocampal CA1 neuronal loss. Pre-treatment with 17β-estradiol ameliorates, in part, ischemia-induced damage in young animals. Because stroke and cardiac arrest are more likely to occur among elderly individuals, neuroprotective studies in older animals have compelling clinical relevance. We investigated whether estradiol would attenuate ischemia-induced hippocampal neuronal injury in middle-aged (12–14 months) male, intact female, ovariectomized (OVX) female and OVX females treated for 14 days with estradiol. Core temperature telemetry probes were also implanted at the time that estradiol was initiated. Ischemia was induced by bilateral occlusion of the common carotid arteries (5 min), during which time skull temperature was maintained under normothermic conditions. Estradiol blocked the modest spontaneous hyperthermia that normally follows ischemia. However, all four groups exhibited substantial neuronal cell loss in the CA1, assessed at 7 after ischemia. These findings indicate that estradiol pre-treatment under conditions that produce neuroprotection in young animals does not protect against ischemia-induced CA1 cell loss in middle-aged female gerbils. [Copyright &y& Elsevier]

To test whether baboons are capable of implementing selective brain cooling, we measured, every 5 min, the temperature in their hypothalamus, carotid arterial bloodstream, and abdominal cavity. The baboons were unrestrained and exposed to 22°C for 7 days and then to a cyclic environment with 15°C at night and 35°C during the day for a further 7 days. During the latter 7 days some of the baboons also were exposed to radiant heat during the day. For three days, during heat exposure, water was withheld. At no time was the hypothalamus cooler than carotid arterial blood, despite brain temperatures above 40°C. With little variation, the hypothalamus was consistently 0.5°C warmer than arterial blood. At high body temperatures, the hypothalamus was sometimes cooler than the abdomen. Abdominal temperature was more variable than arterial blood and tended to exceed arterial blood temperature at higher body temperatures. Hypothalamic temperature cooler than a warm abdomen is not evidence for selective brain cooling. In species that can implement selective brain cooling, the brain is most likely to be cooler than carotid arterial blood when an animal is hyperthermic, during heat exposure, and also dehydrated and undisturbed by human presence. When we exposed baboons to high ambient temperatures while they were water deprived and undisturbed, they never implemented selective brain cooling. We conclude that baboons cannot implement selective brain cooling and can find no convincing evidence that any primate species can do so. [ABSTRACT FROM AUTHOR]

We conducted two experiments that implicate yawning as a thermoregulatory mechanism. The first experiment demonstrates that different patterns of breathing influence susceptibility to contagious yawning. When participants were not directed how to breathe or were instructed to breathe orally (inhaling and exhaling through their mouth), the incidence of contagious yawning in response to seeing videotapes of people yawning was about 48%. When instructed to breathe nasally (inhaling and exhaling through their nose), no participants exhibited contagious yawning. In a second experiment, applying temperature packs to the forehead also influenced the incidence of contagious yawning. When participants held a warm pack (46°C) or a pack at room temperature to their forehead while watching people yawn, contagious yawning occurred 41% of the time. When participants held a cold pack (4°C) to their forehead, contagious yawning dropped to 9%. These findings suggest that yawning has an adaptive/functional component that it is not merely the derivative of selection for other forms of behavior. [ABSTRACT FROM AUTHOR]

Abstract: While cocaine''s interaction with the dopamine (DA) transporter and subsequent increase in DA transmission are usually considered key factors responsible for its locomotor stimulatory and reinforcing properties, many centrally mediated physiological and psychoemotional effects of cocaine are resistant to DA receptor blockade, suggesting the importance of other non-DA mechanisms. To explore the role of cocaine''s interaction with Na+ channels, rats were used to compare locomotor stimulatory and temperature (NAcc, temporal muscle and skin) effects of repeated iv injections of cocaine (1 mg/kg) with those induced by procaine (PRO 5 mg/kg), a short-acting local anesthetic with negligible effect on the DA transporter, and cocaine methiodide (COC-MET 1.31 mg/kg), a quaternary cocaine derivative that is unable to cross the blood–brain barrier. While PRO, unlike cocaine, did not induce locomotor activation, it mimicked cocaine in its ability to increase brain temperature following the initial injection and to induce biphasic, down–up fluctuations following repeated injections. This similarity suggests that both these effects of cocaine may be driven by its action on Na+ channels, a common action of both drugs. While COC-MET also did not affect locomotor activity, it shared with cocaine and PRO their ability to increase brain temperature but failed to induce temperature decreases after repeated injections. These findings point toward activation of peripheral Na+ channels as the primary mechanism of rapid excitatory effects of cocaine and inhibition of centrally located Na+ channels as the primary mechanism for transient inhibitory effects of cocaine. DA receptor blockade (SCH23390+eticlopride) fully eliminated locomotor stimulatory and temperature-increasing effects of cocaine, but its temperature-decreasing effects remained intact. Surprisingly, DA receptor blockade also altered the temperature fluctuations caused by PRO and COC-MET, suggesting that some of the central effects triggered via Na+ channels are in fact DA-dependent. Finally, repeated administration of PRO to animals that had previous cocaine experience led to conditioned locomotion and potentiated temperature-increasing effects of this drug. It appears, therefore, that, in addition to the central effects of cocaine mediated via interaction with the DA transporter and potentiation of DA uptake, interaction with peripheral and central Na+ channels is important for the initial physiological and, perhaps, affective effects of cocaine, likely contributing to the unique abuse potential of this drug. [Copyright &y& Elsevier]

While alterations in dopamine (DA) uptake appear to be a critical mechanism underlying locomotor and reinforcing effects of cocaine (COC), many centrally mediated physiological and affective effects of this drug are resistant to DA receptor blockade and are expressed more quickly following an intravenous (i.v.) injection than expected based on the dynamics of drug concentration in the brain. Because COC is also a potent local anesthetic, its rapid action on Na+ channels may be responsible for triggering these effects. We monitored temperatures in the nucleus accumbens, temporal muscle and skin together with conventional locomotion during a single i.v. injection of COC (1 mg/kg), procaine (PRO, 5 mg/kg; equipotential anesthetic dose), a short-acting local anesthetic drug that, like COC, interacts with Na+ channels, and cocaine methiodide (COC-MET, 1.31 mg/kg, equimolar dose), a quaternary COC derivative that is unable to cross the blood–brain barrier. In this way, we explored not only the importance of Na+ channels in general, but also the importance of central vs. peripheral Na+ channels specifically. COC induced locomotor activation, temperature increase in the brain and muscle, and a biphasic temperature fluctuation in skin. Though PRO did not induce locomotor activation, it mimicked, to a greater degree, the temperature effects of COC. Therefore, Na+ channels appear to be a key substrate for COC-induced temperature fluctuations in the brain and periphery. Similar to PRO, COC-MET had minimal effects on locomotion, but mimicked COC in its ability to increase brain and muscle temperature, and induce transient skin hypothermia. It appears therefore that COC's interaction with peripherally located Na+ channels triggers its central excitatory effects manifested by brain temperature increase, thereby playing a major role in drug sensing and possibly contributing to COC reinforcement. [ABSTRACT FROM AUTHOR]

The balance between metabolic heat production, heat removal by blood flow, and heat conductance defines local temperature distribution in a living tissue. Disproportional local increases in blood flow as compared with oxygen consumption during functional brain activity disturb this balance, leading to temperature changes. In this article we have developed a theoretical framework that allows analysis of temperature changes during arbitrary functional brain activity. We established theoretical boundaries on temperature changes and explained how these boundaries depend on physiology (blood flow and metabolism) and external (heat exchange with the environment) experimental conditions. We show that, in regions located deep in the brain, task performance should be accompanied by temperature decreases in regions where blood flow increases (activated regions) and by temperature increases in regions where blood flow decreases (deactivated regions). The sign of temperature effect may be reversed for superficial cortex regions, where the baseline brain temperature is lower than the temperature of incoming arterial blood due to the heat exchange with the environment. Importantly, due to heat conductance, the temperature effect is not localized to the activated region but extends to a surrounding tissue at rest over the distances regulated by the temperature-shielding effect of blood flow. This temperature-shielding effect quantifies the means by which cerebral blood flow prevents "temperature perturbations" from propagating away from the perturbed regions. For small activated regions, this effect also substantially suppresses the magnitude of the temperature response, making it especially important for small animal brains. [ABSTRACT FROM AUTHOR]

Abstract: The effects of the destruction of the medial preoptic area and the lateral preoptic area with N-methyl-d-aspartic acid on sleep–wakefulness, brain temperature and thermoregulation were studied in two groups of male Wistar rats. Electroencephalogram, electrooculogram and electromyogram, along with brain temperature, were recorded for 3 days, prior to the destruction of the medial preoptic area and the lateral preoptic area, and on the 7th and 21st days after the destruction of these areas. The thermoregulatory capacity of the rats was assessed by recording their brain temperature when they were exposed to severe cold (5±1 °C) and heat (37±1 °C) before and after the lesion. Though sleep was decreased after the destruction of both the medial preoptic area and the lateral preoptic area, paradoxical sleep was reduced only by the destruction of the medial preoptic area. Decrease in sleep after the medial preoptic area lesion was brought about by a decrease in the duration of the slow wave sleep episodes and the frequency of paradoxical sleep episodes. Decrease in sleep after the lateral preoptic area lesion was brought about by a decrease in the frequency of slow wave sleep episodes. There was a significant increase in brain temperature after the medial preoptic area lesion but not after the lateral preoptic area lesion. The rats with lesion in the medial preoptic area showed deficits in thermoregulation on exposure to cold, while those with the lateral preoptic area lesion showed deficits in heat defense ability. The present findings suggest that the medial preoptic area and the lateral preoptic area regulate sleep by different modalities and that there is an anatomical segregation of heat and cold defense functions within the basal forebrain. [Copyright &y& Elsevier]

Abstract: Previous studies have shown that one form of neuroplasticity, population spike (PS) potentiation, can be established in the hamster hippocampus at temperatures above 20 °C. Here, we tested three related hypotheses; namely, that in Syrian hamsters: (1) PS potentiation can be elicited below 20 °C and that at any constant temperature, potentiation can be described by a pair of sigmoidal functions matched to input/output curves; (2) potentiation can be partially reversed by depotentiation (a second and distinctive form of neuroplasticity); and (3) tetanus evokes long-term potentiation in slices from animals housed under conditions corresponding to various stages of the annual hibernation cycle. To test these hypotheses, we measured PS amplitudes and fEPSP slopes in CA1 pyramidal cells in hippocampal slices. We found that sigmoidal functions before and after tetanus showed PS enhancement at 18 °C and a larger enhancement at 28 °C, thereby supporting hypothesis 1. We also found that low-frequency stimulation reduced the amplitude of the potentiated PS by ∼29% at both 18 °C and 28 °C, consistent with hypothesis 2; and that slices from nonhibernating hamsters on long and short photoperiods and from hamsters in hibernation all showed at least 40% increases in fEPSP slope following tetanus at a slice temperature of 23 °C, supporting hypothesis 3. Thus, bidirectional plasticity is present in hamsters. That is, both potentiation and depotentiation were readily evoked at 28 °C; potentiation was muted, while depotentiation (the reversal of the potentiation) remained robust at 18 °C. Moreover, potentiated responses could be elicited in slices from animals housed under diverse conditions. [Copyright &y& Elsevier]

Abstract: The neuroprotective potential of mGluR1 and mGluR5 antagonists (group I), EMQMCM and MTEP, respectively was studied using the 3min forebrain ischemia model in Mongolian gerbils and the hypoxia–ischemia model in 7-day-old rats. Hypoxia–ischemia was induced by unilateral carotid occlusion followed by 75min exposure to hypoxia (7.3% O2 in N2), forebrain ischemia in gerbils was evoked by bilateral common carotid artery occlusion. The postischemic rectal body temperature in rat pups or brain temperature of gerbils was measured. The drugs were administered i.p. three times every 2h after the insult, each time in equal doses of 1.25, 2.5 or 5.0mg/kg. After 2 weeks brain damage was evaluated as weight decrease of the ipsilateral hemisphere in the rat pups or damage to CA1 pyramids in the gerbil hippocampus. The results demonstrated a dose dependent neuroprotection in both ischemic models by EMQMCM, while MTEP was neuroprotective only in the gerbil model of forebrain ischemia. EMQMCM reduced postischemic hyperthermia in gerbils. Thus, the antagonists of mGluR1 and mGluR5 show differential neuroprotective ability in two models of brain ischemia. Postischemic hypothermia may be partially involved in the mechanism of neuroprotection following EMQMCM in gerbils. [Copyright &y& Elsevier]

Abstract: In this study we tested the effect of antagonists of two subtypes of the group I metabotropic glutamate receptors (mGluRs GI) on the induction of ischemic tolerance in relation to brain temperature. These experiments were prompted by indications that glutamate receptors may participate in the mechanisms of ischemic preconditioning. The role of NMDA receptors in the induction of ischemic tolerance has been debated while there is lack of information concerning the involvement of mGluRs GI in this phenomenon. The tolerance to injurious 3min forebrain ischemia in Mongolian gerbils was induced 48h earlier by 2min preconditioning ischemia. Brain temperature was measured using telemetry equipment. EMQMCM and MTEP, antagonists of mGluR1 and mGluR5, respectively, were injected i.p. at a dose of 5mg/kg. They were administered either before preconditioning ischemia in a single dose or after 2min ischemia three times every 2h. Both antagonists did not inhibit the induction of ischemic tolerance. Thus, our data indicate that group I metabotropic glutamate receptors do not play an essential role in the induction of ischemic tolerance. [Copyright &y& Elsevier]

Abstract: Although brain metabolism consumes high amounts of energy and is accompanied by intense heat production, brain temperature is usually considered a stable, tightly “regulated” homeostatic parameter. Current research, however, revealed relatively large and rapid brain temperature fluctuations (3–4 °C) in animals during various normal, physiological, and behavioral activities at stable ambient temperatures. This review discusses these data and demonstrates that physiological brain hyperthermia has an intra-brain origin, resulting from enhanced neural metabolism and increased intra-brain heat production. Therefore, brain temperature is an important physiological parameter that both reflects alterations in metabolic neural activity and affects various neural functions. This work also shows that brain hyperthermia may be induced by various drugs of abuse that cause metabolic brain activation and impair heat dissipation. While individual drugs (i.e., heroin, cocaine, methamphetamine, MDMA) have specific, dose-dependent effects on brain and body temperatures, these effects are strongly modulated by an individual''s activity state and environmental conditions, and change dramatically during the development of drug self-administration. Thus, brain thermorecording may provide new information on the central effects of various addictive drugs, drug–activity–environment interactions in mediating drugs'' adverse effects, and alterations in metabolic neural activity associated with the development of drug-seeking and drug-taking behavior. While ambient temperatures and impairment of heat dissipation may also affect brain temperature, these environmental conditions strongly potentiate thermal effects of psychomotor stimulant drugs, resulting in pathological brain overheating. Since hyperthermia exacerbates drug-induced toxicity and is destructive to neural cells and brain functions, use of these drugs under activated conditions that restrict heat loss may pose a significant health risk, resulting in both acute life-threatening complications and chronic destructive CNS changes. [Copyright &y& Elsevier]

Effects of high and moderate affinity uncompetitive NMDA receptor antagonists (+)MK-801 and memantine on ischemic tolerance were compared in relation to telemetrically controlled brain temperature. The tolerance to an injurious 3 min test of global forebrain ischemia in Mongolian gerbils was induced 48 h earlier by 2 min preconditioning ischemia. Normothermic preconditioning was virtually harmless, and greatly reduced neurode-generation evoked by test ischemia. In hyperther-mic animals it was injurious and failed to induce tolerance. Memantine (5 mg/kg) and (+)MK-801 (3 mg/kg) injected i.p. 1 h before preconditioning did not inhibit ischemic tolerance in the normo-thermic gerbils, while in hyperthermic animals treated with (+)MK-801 ischemic tolerance was partially restored. Subchronic 3 day infusion of memantine (30 mg/kg/day) significantly decreased neurodegeneration, and preconditioning in the nor-mothermic gerbils further reduced neuronal damage. Hyperthermia exacerbated preconditioning ischemia and in this way reduced expression of tolerance, while (+)MK-801 partially reversed this effect. Our results do not confirm previous reports on the role of NMDA receptors in the induction of ischemic tolerance in gerbils. [ABSTRACT FROM AUTHOR]

The suprachiasmatic nucleus (SCN) regulates the circadian rhythms of body temperature (Tb) and vigilance states in mammals. We studied rats in which circadian rhythmicity was abolished after SCN lesions (SCNx rats) to investigate the association between the ultradian rhythms of sleep-wake states and brain temperature (Tbr), which are exposed after lesions. Ultradian rhythms of Tbr (mean period: 3.6 h) and sleep were closely associated in SCNx rats. Within each ultradian cycle, nonrapid eye movement (NREM) sleep was initiated 5 ± 1 min after Tbr peaks, after which temperature continued a slow decline (0.02 ± 0.006°C/min) until it reached a minimum. Sleep and slow wave activity (SWA), an index of sleep intensity, were associated with declining temperature. Cross-correlation analysis revealed that the rhythm of Tbr preceded that of SWA by 2–10 min. We also investigated the thermoregulatory and sleep-wake responses of SCNx rats and controls to mild ambient cooling (18°C) and warming (30°C) over 24-h periods. SCNx rats and controls responded similarly to changes in ambient temperature. Cooling decreased REM sleep and increased wake. Warming increased Tbr, blunted the amplitude of ultradian Tbr rhythms, and increased the number of transitions into NREM sleep. SCNx rats and controls had similar percentages of NREM sleep, REM sleep, and wake, as well as the same average Tb within each 24-h period. Our results suggest that, in rats, the SCN modulates the timing but not the amount of sleep or the homeostatic control of sleep-wake states or Tb during deviations in ambient temperature. [ABSTRACT FROM AUTHOR]

Abstract: Brain temperatures (T br) of male Wistar rats were recorded at every 15min interval for 24h, prior to the destruction of the medial septal (MS) neurons with N-methyl-d-aspartic acid, and on the 7th, 14th and 21st days after the destruction. The capacity of the rats to regulate their body temperature under severe cold and heat was assessed by recording their T br when they were exposed to 5±1 and 37±1°C for 2h, before lesion and on 8th, 9th, 15th, 16th, 22nd and 23rd days after the lesion. The T br was decreased and its circadian variation increased after the MS lesion. On exposure to an ambient temperature of 5±1°C the T br was decreased on 9th and 16th days after the lesion, when compared with the sham lesion group on identical days, though the fall in temperature was not significant on the 23rd day. The change in T br (compared with the sham lesion group) was not significantly different on all days of exposure to 37±1°C. The decrease in T br after the MS lesion is in contrast to the hyperthermia produced by lesion of the adjoining thermoregulatory areas. The present findings suggest that the MS lesions caused an alteration in the set point of body temperature, without drastic changes in thermoregulatory ability. [Copyright &y& Elsevier]

Homeotherm state can bear a relationship to development of self-cognitive consciousness in evolution. Both explicit memory and consciousness could arise from sleep and dreams. In evolution several biomolecular and biophysical mechanisms have been developed, which made possible the formation of strong coherence of the information system in the brain. This coherence can serve as a basis of explicit holograph-like information system in the brain. This article, although not going into details about neuromolecular, biophysical or biophoton processes, proposes a relationship between thermoregulation and biophysical (biophoton) informational processes in the cells of the brain, it does not claim to solve the secret of consciousness, but points out that biophotons play an important role in information processes of the brain during sleep, dreams and wakefulness, and the brain can operate by pictures during thinking. [ABSTRACT FROM AUTHOR]

Abstract: Alterations in sleep induced by chronic exposure to mild changes in ambient temperature (T a) were studied in male Wistar rats with chronically implanted electrodes for recording electrooculogram (EOG), electroencephalogram (EEG) and electromyogram (EMG), and a thermocouple to record the brain temperature (T br). Changes in sleep–wakefulness (S–W) and T br on exposure to warm (30±1 °C) and cold (18±1 °C) T a for 4 weeks were studied in two groups of five rats each. Chronic heat exposure produced a persistent increase in sleep, primarily due to an increase in the durations of sleep episodes. A disproportionate increase in sleep during the dark period resulted in reduced circadian variation. The paradoxical sleep (PS)/total sleep time (TST) ratio also remained increased, during heat exposure. On chronic cold exposure, the sleep was decreased initially, but it recovered after 3 weeks, due to an increase in the frequency of slow wave sleep (SWS) episodes. The T br was not altered on exposure to warm T a, but it remained high throughout the 4 weeks of cold exposure. The increase in the amount of sleep, especially the PS with enhanced ambient temperature, may be considered as an adaptation to thermal load aimed at energy conservation. Though the increased wakefulness is suggested to enable the organism to optimize thermoregulation during acute cold stress, thermoregulation itself may be readjusted to ensure homeostatic restoration of sleep during chronic cold exposure. [Copyright &y& Elsevier]

To determine the relationships among plasma ghrelin and leptin concentrations and hypothalamic ghrelin contents, and sleep, cortical brain temperature (Tcrt), and feeding, we determined these parameters in rats in three experimental conditions: in free-feeding rats with normal diurnal rhythms, in rats with feeding restricted to the 12-h light period (RF), and in rats subjected to 5-h of sleep deprivation (SD) at the beginning of the light cycle. Plasma ghrelin and leptin displayed diurnal rhythms with the ghrelin peak preceding and the leptin peak following the major daily feeding peak in hour 1 after dark onset. RF reversed the diurnal rhythm of these hormones and the rhythm of rapid-eye-movement sleep (REMS) and significantly altered the rhythm of Tcrt. In contrast, the duration and intensity of non-REMS (NREMS) were hardly responsive to RF. SD failed to change leptin concentrations, but it promptly stimulated plasma ghrelin and induced eating. SD elicited biphasic variations in the hypothalamic ghrelin contents. SD increased plasma corticosterone, but corticosterone did not seem to influence either leptin or ghrelin. The results suggest a strong relationship between feeding and the diurnal rhythm of leptin and that feeding also fundamentally modulates the diurnal rhythm of ghrelin. The variations in hypothalamic ghrelin contents might be associated with sleep-wake activity in rats, but, unlike the previous observations in humans, obvious links could not be detected between sleep and the diurnal rhythms of plasma concentrations of either ghrelin or leptin in the rat. [ABSTRACT FROM AUTHOR]

Drugs of abuse, such as 3,4-methylenedioxymethamphetamine (MDMA), often have more powerful effects during states of increased activation and under specific environmental conditions. Because hyperthermia is a major complication of MDMA use and a factor potentiating neurotoxicity, we examined the effects of this drug (9 mg/kg, sc; approximately one-fifth of the known LD50 in rats) on brain [nucleus accumbens (Nacc) and hippocampus (Hippo)] and muscle (musculus temporalis) temperatures in male rats under conditions that either model human drug use (social interaction with female, warm temperature) or restrict heat dissipation from the brain (chronic occlusion of jugular veins). Under quiet resting conditions at 23 °C, MDMA induced a moderate but prolonged hyperthermia. Both NAcc and Hippo showed more rapid and stronger temperature increases than muscle, suggesting metabolic neural activation as a primary cause of brain hyperthermia. During social interaction with a female, brain hyperthermia induced by MDMA was significantly potentiated (+89%). Brain hyperthermia induced by MDMA was also strongly potentiated (+188%) in animals with chronically occluded jugular veins, suggesting impaired cerebral outflow enhances intrabrain heat accumulation. At 29 °C, MDMA pushed temperatures in the brain to its biological limits (>41 °C; +268%), resulting in fatalities in most (83%) tested animals. Therefore, by inducing metabolic brain activation and restricting heat dissipation, MDMA use under ‘party’ conditions may be much more dangerous than under standard laboratory conditions. [ABSTRACT FROM AUTHOR]

Introduction: Accurate knowledge of cerebral temperature is assuming increasing importance, because its manipulation is employed more frequently for cerebral protection. Purpose: This prospective clinical study was performed to examine how well intraventricular temperature reflects global cerebral temperature. Methods: The intraventricular temperature was monitored in 61 patients who were admitted to the neurointensive care unit for various intracranial pathological entities. A temperature probe coupled to an intraventricular pressure monitor was inserted in the lateral ventricle. At the conclusion of the monitoring process, a second intraventricular temperature probe was inserted in the ipsilateral ventricle and the previous one was carefully and gradually removed. During that removal, the intraparenchymal temperature was monitored for 90 minutes at 1-cm intervals throughout the brain parenchyma. Results: The mean intraventricular temperature was 37.84±1.03°C, whereas the mean systemic (rectal) temperature was 37.65±0.68°C. At 1 cm outward distance from the lateral ventricle, the mean intraparenchymal temperature was 38.21±0.32°C, 38.39±0.33°C at 2 cm, 38.27± 0.31°C at 3 cm, 38.26±0.29°C at 4 cm, and, finally, 37.9±0.50°C at 5 cm. Statistical analysis of the recordings showed no statistically significant differences between the intraventricular and intraparenchymal temperatures and intraventricular and rectal temperatures. No statistically significant correlation was established between the intraventricular temperature and parameters, such as the patient’s age, sex, and admitting diagnosis. Conclusion: Cerebral temperature was relatively stable through the brain parenchyma in this study. Because intraventricular temperature accurately reflects cerebral temperature, this is a reasonable monitoring site for cerebral temperature analysis. [ABSTRACT FROM AUTHOR]

We previously reported that rats exposed to neonatal hypoxic-ischemic (HI) insult showed selective and long-lasting learning and memory impairments in the plus maze, 8-arm radial maze, choice reaction time (CRT) task, and water maze, and that they showed severe brain injury to areas such as parietal cortex, hippocampus, striatum and thalamus. In this study, we examined the effects of hypothermia and hyperthermia on learning and memory deficits following neonatal HI insult. Seven-day-old Wistar rats were subjected to left carotid artery ligation followed by 2 h of hypoxia (8% O2/92% N2) under three different temperature conditions: 27 °C (hypothermia), 33 °C (normothermia) and 37 °C (hyperthermia) in temperature-controlled chambers. Hypothermia significantly reduced attentional deficits in the CRT task and spatial learning deficits in the water maze, and protected against severe brain injury in comparison with the control temperature. On the other hand, hyperthermia aggravated the behavioral deficits and brain injury. These outcomes clearly show that temperature regulation during HI insult plays an important role in the induction of behavioral and histological changes following neonatal HI insult in rats. [Copyright &y& Elsevier]

While it is generally assumed that cocaine self-administration (SA) is determined and maintained by the pharmacological actions of cocaine in the brain, it is also a drug-motivated and drug-reinforced goal-directed behavior, which is determined by concurrent learning and behavioral performance. To dissociate the contributions of pharmacological and behavioral factors to cocaine SA, it is important to compare cocaine SA with its pharmacological copy, passive intravenous (iv) cocaine administration. This approach was employed in the present study with respect to brain temperatures, a dynamic parameter that reflects metabolic neural activity and shows consistent fluctuations during cocaine SA. Passive cocaine injections performed with the same dose/pattern as SA induced brain temperature fluctuations similar in many ways to those in behaving animals. The initial passive drug administration of a session elevated brain temperature, while subsequent repeated injections were associated with biphasic temperature fluctuations that maintained at a relatively stable plateau. Although the magnitude of these fluctuations was twofold smaller than in behaving animals, passive animals had the same pattern; brain temperatures transiently decreased after cocaine injection, then increased, and were inhibited again by the next cocaine infusion. In contrast to self-administering animals, rats exposed to passive cocaine injections had significantly lower basal temperatures and never showed gradual temperature increases preceding the initial injection. Striking differences in brain temperature dynamics seen in the beginning of a session suggest that during the development of drug-taking behavior the initial cocaine-induced neural activation becomes transformed into behavior-related “anticipatory” neural activation (motivational arousal) that fuels drug seeking and results in the initial drug intake. While this activation is triggered by drug-related cues and enhanced by the initial cocaine intake, subsequent highly cyclical cocaine intakes appear to be primarily pharmacologically determined. [Copyright &y& Elsevier]

Because neural activity is highly energy consuming and heat producing, brain temperature offers a reliable, real-time measure of an animal''s activity state and its changes induced by environmental and drug challenges. Therefore, it allows evaluation of the activity state of an animal preceding drug administration and its relation to subsequent drug-induced neural effects. This approach was used to explore the state dependency of cocaine''s effects. Brain and body temperatures, as well as locomotion were measured simultaneously in rats during repeated, daily administration of cocaine (15 mg/kg ip, daily for 5 days) under different experimental conditions. The drug was administered via (a) a chronically implanted catheter in quiet resting conditions, (b) an injection made under quiet rest or (c) an injection under activated conditions associated with placement in the cage. Although brain temperature and movement increased after cocaine administration in each condition, cocaine''s action (evaluated as cocaine–saline difference for both parameters) was situational. Catheter-administered cocaine induced the strongest movement activation and robust, monophasic temperature increase, which remained relatively stable following each subsequent drug infusion. Cocaine injected during quiet and, especially, activated conditions, induced a weaker locomotor activation, while the temperature response (evaluated as drug–saline difference) had a biphasic pattern. Cocaine initially inhibited the temperature increases seen in saline-treated animals (0–20 min) and then induced a more prolonged hyperthermia, which was about twofold weaker than that seen after catheter-administered drug. Although movement activation gradually increased following repeated treatment in activated conditions, the magnitude of this sensitized motor response barely reached the levels induced by the initial cocaine administration via catheter. These data suggest that both the acute effects of cocaine in the brain and their change following repeated drug administration are dependent upon the ongoing neural activity state of the animal. Cocaine''s interaction with this activity state is a crucial factor determining the behavioral effects of this drug, including state-dependent motor sensitization. [Copyright &y& Elsevier]

Since the metabolic activity of neural cells is accompanied by heat release, brain temperature monitoring provides insight into behavior-associated changes in neural activity. In the present study, local temperatures were continuously recorded in several brain structures (nucleus accumbens, medial–preoptic hypothalamus and hippocampus) and a non-locomotor head muscle (musculus temporalis) in a receptive female rat during sexually arousing stimulation and subsequent copulatory behavior with an experienced male. Placement of the male into a neighboring compartment increased the female''s temperature (∼0.8 °C) and additional, transient increases (∼0.2 °C) occurred when the rats were allowed to see and smell each other through a transparent barrier. Temperatures gradually increased further as the male repeatedly mounted and achieved intromissions, peaked 2–3 min after male''s ejaculation (0.2–0.4 °C), and abruptly dropped until the male initiated a new copulatory cycle. Similar biphasic fluctuations accompanied subsequent copulatory cycles. Although both arousal-related temperature increases and biphasic fluctuations associated with copulatory cycles were evident in each recording location, brain sites showed consistently faster and stronger increases than the muscle, suggesting metabolic brain activation as the primary source of brain temperature fluctuations and a force behind associated changes in brain temperature. Robust brain hyperthermia and the generally similar pattern of phasic temperature fluctuations associated with individual events of sexual interaction found in males and females suggest widespread neural activation (motivational arousal) as a driving force underlying this cooperative motivated behavior in animals of both sexes. Females, however, showed different temperature changes in association with the initial (first mount or intromission) and final (ejaculation) events of each copulatory cycle, suggesting sex-specific differences in neural activity associated with the initiation and regulation of sexual behavior. [Copyright &y& Elsevier]

: BackgroundTemperature reversal, which is defined as observation of higher brain temperature than systemic temperature followed by lower brain temperature than systemic temperature, implies a poor prognosis in patients with severe subarachnoid hemorrhage (SAH). Serial regional cerebral blood flow (CBF) imaging using single-photon emission tomography (SPECT) was performed in 2 patients with severe SAH who showed temperature reversal.: Case description54-year-old woman and a 55-year-old man with severe SAH underwent ventricular drainage using a catheter that allowed monitoring of the brain temperature. SPECT imaging in these two patients showed that CBF was preserved before the occurrence of the temperature reversal and was exhausted afterwards. These patients died within 2 to 3 days.: ConclusionsTemperature reversal may indicate the exact time when absence of brain perfusion occurs, causing irreversible brain damage. [Copyright &y& Elsevier]

: BackgroundThe significance of brain temperature (BT) in patients with severe brain damage remains unclear. This study investigated the relationships between BT, systemic temperature (ST), and clinical outcome in patients with severe subarachnoid hemorrhage.: MethodsThirty-one comatose patients with severe subarachnoid hemorrhage underwent ventricular drainage immediately after admission. The ventricular catheter also allowed monitoring of BT. ST was continuously measured using a bladder catheter with thermistor probe.: ResultsBT at the start of the monitoring was lower than ST in four patients, and all died of brain swelling. BT was higher than ST at first but later fell below ST (“temperature reversal”) in 12 patients, who all died of acute brain swelling. BT was higher than ST throughout the monitoring in 15 patients. Five of these patients died of causes other than brain swelling such as rerupture of the cerebral aneurysm, multiple organ failure, or respiratory failure. The other 10 patients survived with various degrees of disability.: ConclusionsObservation of BT and ST can predict the outcome of severe subarachnoid hemorrhage. [Copyright &y& Elsevier]

The purpose of the study was to identify extracranial locations in which temperature changes in humans reflect those of intracranial temperature in a reliable and repeatable way. This was achieved by subjecting 14 non-anaesthetized patients after neurosurgery to face fanning while intracranial and extracranial temperatures were continuously measured. In all patients the cranium was closed and the group included both febrile and non-febrile as well as hyperthermic and normothermic patients. The patients' faces were fanned for 20–30 min, with a small fan at an air speed of 3.25 m s-1. This gave intracranial temperature changes measured in the subdural space (Tsd) that were highly and significantly correlated (r=0.91, P<0.05, n=14) with changes in tympanic temperatures (Tty). A low, statistically insignificant correlation (r=0.40, P>0.05, n=12) was found between Tsd and oesophageal temperatures. In conclusion, intracranial temperature changes, induced by face fanning, were reliably reflected by the changes in Tty. [ABSTRACT FROM AUTHOR]

Summary. Background: The purpose of the present study was to examine the influence of cooling and rewarming conditions using an accurate brain temperature control system. Method: The brain temperature of animals was measured with a thermometer while feedback regulation was achieved with a cold (4°C) and hot (50°C) water on-off flow system. Brain temperature was well controlled throughout the experiment by using both cold water and hot water simultaneously. Three groups were studied, as follows: 1) the standard group (cooled to 24°C for 1 hour, kept at 24°C for 2 hours and rewarmed to 37°C for 1 hour), 2) the rapid-cooling group (cooled to 24°C for 30 min, kept at 24°C for 2 h, and rewarmed to 37°C for 1 h), 3) the rapid-rewarming group (cooled to 24°C for 1 h, kept at 24°C for 2 h, and rewarmed to 37°C for 30 min) and the normal-control group. Findings: An increase of MAP-2 immunoreactivity of the CA1 neurons in the dorsal hippocampus was observed one week but not one month after hypothermia in the rapid-rewarming group. There was also a significant increase in the glutamate and lactate value at the end of rewarming compared with the baseline in the rapid-rewarming group (p<0.01). Interpretation: Our results suggest that rapid rewarming after hypothermia triggered an uncoupling of cerebral circulation and metabolism, inducing an increase of extracellular glutamate and lactate, consequently reversible neuronal cell damage. [ABSTRACT FROM AUTHOR]

Abstract Background: Although selective brain hypothermia is expected to be a promising neuroprotective treatment, the thermal distribution under hypothermia is not fully investigated. We applied selective head cooling to seven newborn piglets under general anesthesia in order to investigate the mechanism of cooling. Methods: Seven healthy, large white piglets aged within 5 days after birth were studied. Temperatures were monitored at the superficial brain (0.5 cm), deep brain (2.0 cm), scalp skin, nasopharynx, tympanum, esophagus, and rectum. A radiant heater and a warmer blanket were used to maintain the normal rectal temperature (38.5-39°C). For the first piglet, the coolant temperature was widely changed from 15C to - 20C in order to define the practical range. Subsequently, the coolant temperature was set at 10C, 0C, and - 10C for the remaining six piglets. The target deep brain temperature was set at 35C, as the same reduction of brain temperature might provide moderate brain hypothermia in the human neonate. Results: With 0C coolant temperature, the deep brain temperature was cooled to 35C; however, the scalp skin attached to the cooling cap became broadly blotchy and injured in all animals. When we induced minimal systemic hypothermia by 1C for a cohort of three piglets, the deep brain temperature decreased in parallel with the rectal temperature, which enabled us to achieve the target temperature with 10°C coolant without injuring the scalp skin. The scalp skin and nasopharyngeal temperatures were good predictors of both superficial and deep-brain temperatures throughout the experiment. Conclusions: Our results suggest that moderate brain hypothermia may be applied to newborn infants without inducing moderate systemic hypothermia. [ABSTRACT FROM AUTHOR]

Because focal seizures produce an increase in local cerebral metabolism and blood flow, we wanted to determine whether they might lead to changes in brain temperature. We induced focal neocortical seizures by microinjection of 4-aminopyridine (4-AP) into the rat motor cortex. The temperature on the dura immediately over the injection site, or 8 mm away, was measured with a thermocouple and in some experiments relative blood flow was monitored with a laser Doppler probe. In animals that did not receive 4-AP, brain and rectal temperature remained fairly constant at 33.5 and 37.2 °C, respectively, over a 2 h monitoring period. In animals treated with 4-AP, brain temperature over the seizure focus rose an average of 0.3 °C, within a few seconds of seizure onset, while rectal temperature remained constant. The seizure-induced temperature rise was preceded by an increase in cortical blood flow. The temperature, but not blood flow, was also elevated 8 mm away from the seizure focus. When blood flow was increased independently of neuronal activity, by elevating pCO2, brain temperature also rose by about 0.3 °C. Focal seizures in anesthetized rats produce a small, but statistically significant increase in local brain temperature, as a result of increased blood flow that brings brain temperature closer to body temperature. In humans, seizures could actually cause a reduction in brain temperature, because brain temperature is normally higher than body temperature. [Copyright &y& Elsevier]