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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arousal at birth is likely to be accompanied by changes in gene expression patterns in the brain. We analyzed the expression levels of genes that may be involved in neonatal adaptation. We have also tried to dissect the effect of hypoxia and hypothermia, two components that may play a role in gene expression at birth. Therefore, we analyzed the expression patterns of the c-fos, tyrosine hydroxylase, enkephalin, preprotachykinin-A, and neuropeptide Y genes in various brain regions of rat pups at various time points after cesarean section under normal conditions and after exposure to hypoxia and hypothermia. We found that c-fos RNA was up-regulated transiently after birth in neocortex, midbrain, and pons-medulla with a maximum of 30 min after cesarean section, and that this transient increase was not further augmented by hypoxia and hypothermia. The expression patterns of the other genes were not significantly altered, with the exception of a very slight increase in tyrosine hydroxylase RNA levels. We discuss tentative mechanisms for the transient increase in c-fos expression and the possible involvement of catecholamines in this process.
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PMID:Expression of c-fos, tyrosine hydroxylase, and neuropeptide mRNA in the rat brain around birth: effects of hypoxia and hypothermia. 770 Jul 28

Acute stress is known to evoke a discrete pattern of c-fos expression in the brain. The work reported here shows that this pattern is modified in regionally specific ways following repeated stress, and that this can be correlated with changes in telemetered heart rate, core temperature and corticosterone output that occur during adaptation. Intact male rats were restrained for 60 min daily for one or 10 days. Stress-induced tachycardia was maximal 10 min following the onset of restraint, and decreased thereafter. The peak value was not altered by repeated restraint, but levels fell towards baseline values more rapidly with increasing bouts of stress. Core temperature showed marked reduction during the first 10 min of the initial stress, followed by a minor (and not very consistent) overshoot during the remainder of the stress period. In contrast to heart rate, stress-induced hypothermia did not alter during repeated restraint. Corticosterone was raised dramatically immediately following the first 60-min session of restraint, and this was attenuated by repeated stress. Sixty minutes after the end of the first stress session, there was pronounced c-fos expression in the lateral septum, lateral preoptic area, lateral hypothalamic area, all divisions of the hypothalamic paraventricular nucleus, the medial (but not central) amygdala, the locus ceruleus and a brainstem structure (thought to be Barrington's nucleus), compared to rats transferred to the testing room but not restrained. Sixty minutes after the 10th stress session, c-fos expression was markedly decreased in some of these areas compared with the pattern observed after the first stress, especially in the paraventricular nucleus (dorsal and medial parvicellular regions) and in medial amygdala. However, all other areas measured demonstrated a sustained response even after repeated stress. There were no significant differences in c-fos expression in rats repeatedly transferred to the testing room (but not stressed) compared to singly transferred counterparts. These results show that both neuronal and physiological responses adapt to a repeated stress, but that in both cases this has highly specific components. It seems likely that adaptive changes in c-fos expression are associated with those in some features of autonomic and endocrine reactions. It is noteworthy that there is evidence that the lateral septum, in which c-fos expression did not diminish after repeated stress, may be involved in temperature control, whereas the paraventricular nucleus, in which c-fos did alter, has been linked with both cardiac and corticoid regulation.
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PMID:Regional changes in c-fos expression in the basal forebrain and brainstem during adaptation to repeated stress: correlations with cardiovascular, hypothermic and endocrine responses. 771 80

We have shown previously that repeated restraint stress results in differential adaptation at both macrophysiological and cellular levels. Chronic stress accentuates vasopressinergic control of adrenocorticotropic hormone secretion in the pituitary. The present work determined whether endogenous vasopressin plays a role in response to repeated restraint. The first experiment explored changes in the response of repeatedly stressed animals to intracerebral vasopressin infusions. The second determined the effect of pretreating rats with a vasopressin V1a receptor antagonist on the way that they adapted to repeated restraint. Experiment 1: rats were subjected either to daily 60-min restraint for 10 days or transferred to the testing room where restraint sessions took place (controls). On the 11th day, they were infused with either artificial cerebrospinal fluid or 250 pmol vasopressin. The behavioural response to vasopressin was unaltered by previous stress. Plasma corticosterone was lowered in vasopressin-treated rats only after previous stress. Sixty minutes after vasopressin infusion, the central amygdala, locus coeruleus, the nucleus of the solitary tract and the dorsal vagal nucleus expressed increased levels of c-fos, and there were significant two-way interactions between stress and infusion for dorsal paraventricular nucleus, locus coeruleus and dorsal vagal nucleus. One-way analysis suggested that previous stress also reduced the c-fos response to vasopressin in the nucleus of the solitary tract. These results show that previous stress causes differential alterations in behavioural, endocrine and cellular responses to vasopressin. Experiment 2: rats were implanted with a transmitter which monitored heart rate and core temperature and a lateral cerebroventricular cannula. For 10 days, either artificial cerebrospinal fluid or 2500 pmol V1a antagonist, [d(CH2)1(5)-O-Me-Tyr2-Arg8]-vasopressin were infused i.c.v. 10 min prior to a 60-min restraint session. On the 11th day, no infusions were carried out, but rats received the usual period of restraint. The vasopressin antagonist was followed by motor responses (freezing, grooming and burrowing), more evident during the third and fifth days of stress. Core temperature responses were altered by the antagonist: stress-induced hypothermia was greatly reduced. Reduced baseline core temperatures, observed in controls as successive stress proceeded, were absent in antagonist-treated rats. By contrast, there were no significant effects of vasopressin antagonism on stress-induced tachycardia, nor in the way that this adapted to repeated restraint. On the 11th day (no i.c.v. infusions), hypothermic responses were no different in rats previously receiving either antagonist or control vehicle, but secondary hyperthermia was greater in the first group. Corticosterone levels were not altered by previous i.c.v. infusions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alterations in sensitivity to intracerebral vasopressin and the effects of a V1a receptor antagonist on cellular, autonomic and endocrine responses to repeated stress. 771 81

Sixty min supine restraint stress induced a marked, but transient, hypothermic response in intact male rats, which tended to recover towards pre-stress levels or slightly overshoot during the later stages of restraint. Castration reduced the initial hypothermia but increased overshoots. Baseline (pre-stress) core temperature was also higher in castrated than intact rats, but the reduction in stress-induced hypothermia was still present even when this difference had been taken into account. The hypothermic response was not altered during the course of 10 sessions of daily repeated restraint in either intact or castrated rats. Castration did not alter cardiac responses to restraint. Both intact and castrated rats showed marked tachycardia during the initial 12 min of restraint, followed by a gradual fall towards baseline values. Repeated restraint accentuated the second phase of the cardiac response, without modifying the initial tachycardia, in both intact and castrated animals. The response of blood corticosterone levels to the first period of restraint was unaltered by castration but the attenuation observed after 10 sessions of stress was more complete in castrated rats. The neuronal c-fos response 60 min after the last of the series of repeated restraints was less in the hypothalamic paraventricular nucleus, medial amygdala, and locus coeruleus compared with that following the first session, but not in the lateral septum or the bed nucleus of the stria terminalis. Castration did not change the c-fos profile following the same number of restraint sessions. Castration depleted completely the vasopressinergic innervation in the lateral septum, diagonal band of Broca and medial amygdala.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of long-term castration on the neuronal and physiological responses to acute or repeated restraint stress: interactions with opioids and prostaglandins. 776 26

We have previously demonstrated that a single administration of ethanol induces the expression of c-fos mRNA in the hypothalamic paraventricular nucleus (PVN). However, Fos protein must interact with a member of the Jun family to form functional heterodimers. To determine whether ethanol may have differential effects on c-fos and c-jun expression, we injected male rats acclimated to a 25 degrees C environment with ethanol (3 g/kg b.wt.) or saline. Using in situ hybridization histochemistry with oligonucleotide probes, we found that ethanol increased c-fos mRNA in the PVN, but decreased c-jun mRNA both in the PVN and in hippocampus. Considering that ethanol produces hypothermia and that the PVN contains neurons activated during hypothermia, we evaluated the effect of cold on c-fos and c-jun mRNA. Both cold and ethanol increased c-fos mRNA, and the effects were additive. However, c-jun mRNA levels in both PVN and hippocampus were unaffected by temperature. Finally, c-jun mRNA levels in the hippocampus were significantly reduced by chronic ethanol exposure, and this trend was also observed in the PVN. These findings demonstrate that a single injection of ethanol has opposite effects on the expression of nuclear transcription factors which interact to regulate gene expression in the nervous system.
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PMID:A single administration of ethanol simultaneously increases c-fos mRNA and reduces c-jun mRNA in the hypothalamus and hippocampus. 796 56

Transient global ischaemia induces the expression of immediate early genes. Using in situ hybridization, the expression of c-fos, fosB, fra-1, fra-2, c-jun and junB was studied after 15 min of normothermic and hypothermic (33 degrees C) transient forebrain ischaemia in the rat, induced by common carotid occlusion combined with systemic hypotension. Two phases of induction of the immediate early genes were observed. The early phase, peaking at 1-2 h of reperfusion, was dominated by marked expression in the dentate gyrus. The second phase, with maximal expression at 12-36 h of reperfusion, was observed particularly in the vulnerable CA1 and CA3 regions. Hypothermia increased the early induction of one of the genes studied, signifying a differential effect of hypothermia upon the signal transduction mechanisms activating these genes. The late induction occurred earlier after hypothermic than after normothermic ischaemia. The early expression of immediate early genes is due to the rapid activation of cytosolic response elements caused by the ischaemic insult. We suggest that the late induction is a stress signal for activation of repair processes, analogous to the cellular response seen after UV light-induced DNA damage. The relatively fast induction of the immediate early genes following hypothermic ischaemia may reflect a faster resumption of normal intracellular signalling, enhancing neuronal recovery.
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PMID:Biphasic expression of the fos and jun families of transcription factors following transient forebrain ischaemia in the rat. Effect of hypothermia. 854 58

Despite the importance of pediatric anesthesiology, the sites and mechanisms of anesthetic action in the neonate are not well described in either human or nonhuman species. This experiment investigated suppression produced by different anesthetic agents of neuronal activity in the lumbar spinal cord of the 3-day-old rat. The expression of the c-fos immediate early gene following formalin injection into the hindpaw was used as a marker for neuronal activity. Pups were anesthetized by one of the following often-used agents: methoxyflurane, acepromazine, a mixture of ketamine and xylazine, and hypothermia. All treatments induced behavioral anesthesia. Despite the behavioral anesthesia, the ketamine-xylazine mixture was completely ineffective in suppressing formalin-induced-Fos expression. In contrast, methoxyflurane and hypothermia blocked the appearance of the Fos protein. Similarly, acepromazine was effective in eliminating some of the Fos-labeled nuclei. These data suggest that, in the infant rat, both hypothermia and methoxyflurane act in part at the spinal level by depressing either primary afferents or dorsal horn neuronal activity whereas the site of action for ketamine-xylazine may be located supraspinally.
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PMID:The suppression of formalin-induced fos expression by different anesthetic agents in the infant rat. 887 23

The endogenous tridecapeptide neurotensin exerts a wide range of behavioral, electrophysiological and neurochemical effects when administered directly into the brain. These effects are thought to result from the activation of distinct populations of neurotensin receptors distributed throughout the central nervous system. We have mapped the sites of functional change in the rat brain associated with the central administration of neurotensin using the induction of the nuclear protein products of the immediate early genes c-fos and zif268 as markers of cellular activation. The administration of neurotensin into the lateral ventricle of rats produced an increase in the number of nuclei positive for Fos and Zif268 immunoreactivity in the central and basolateral nuclei of the amygdala and the paraventricular and supraoptic nuclei of the hypothalamus. Neurotensin also produced an increase in serum corticosterone concentration and decrease in body temperature. The intraperitoneal administration of SR48692, a non-peptide neurotensin receptor antagonist, blocked the neurotensin-induced corticosterone secretion and significantly reduced the number of neurotensin-induced Fos-positive and Zif268-positive neurons in the amygdaloid complex. A significant positive correlation was found between the number of Fos-positive nuclei in the central or basolateral nucleus of the amygdala and the serum corticosterone concentration. A significant positive correlation was also found between the number of Zif-positive cells in the paraventricular nucleus of the hypothalamus and change in body temperature following treatment. Our findings indicate that the central role of neurotensin in increasing serum corticosterone involves the induction of Fos in the central and basolateral nuclei of the amygdala. In contrast, the neurotensin-induced hypothermia, which was unaffected by pretreatment with SR48692, involves Zif induction in the paraventricular nucleus of the hypothalamus. These data support further the existence of central neurotensin receptor subtypes which may regulate distinct immediate early genes.
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PMID:Neurotensin induces Fos and Zif268 expression in limbic nuclei of the rat brain. 893 47

Immediate early genes are induced by transient global ischemia. Using immunohistochemistry we studied the effect of intraischemic hypothermia (30 degrees C) on the expression of c-fos and fos-B proteins following 10 min forebrain ischemia in the gerbil. Postischemia (PI) periods of 1 hour (h), 6 h, 1 day (d) and 2 d and nonischemic controls were examined in normothermic and hypothermic brains. In normothermic ischemic brains, marked expression of c-fos occurred in the dentate gyrus after 1 h PI which extended to CA2-4 regions by 6 h. Hypothermia hastened the time course of c-fos expression as it was expressed simultaneously in the dentate gyrus as well as CA2-4 regions after only 1 h, and by 6 h the expression remained only in the CA2-4 regions and not the dentate gyrus in hypothermic ischemic brains. There was no difference in its expression between normothermic and hypothermic brains in the 1 d and 2 d PI animals. Somewhat similar changes were noted in fos-B expression. In normothermic ischemic brains fos-B was induced in the dentate gyrus by 1 h PI, and by 6 h it extended to involve CA1-4 cells. The hypothermic ischemic brains showed faster induction of fos-B so that the dentate gyrus as well as CA1-4 regions were immunopositive at 1 h PI. There was no difference in its expression between normothermic and hypothermic brains in the subsequent PI periods of 6 h, 1 d and 2 d. The shift towards faster sequential induction of these genes by hypothermia in ischemic brains may be indicative of preservation of or faster recovery of mechanisms involved in intracellular signalling.
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PMID:Expression of c-fos and fos-B proteins following transient forebrain ischemia: effect of hypothermia. 901 91

This study had three objectives: (i) to determine whether there were individual differences in the activation and adaptation of a range of immediate-early genes to repeated restraint stress, (ii) to monitor physiological responses (endocrine, cardiovascular and core temperature) and their adaptation with repeated presentations of the stressor, and (iii) to determine whether any of these indices were altered by dehydroepiandrosterone, an anti-glucocorticoid steroid known to be reduced in humans by stress. Four groups of male rats were implanted subcutaneously with either dehydroepiandrosterone or control (paraffin) pellets. They were then subjected to either a single or 14 days of restraint (60 min/day) or transferred to the testing room (unstressed). Repeatedly stressed animals and their controls were also implanted with intra-abdominal telemetric transmitters to record heart rate and core temperature. Protein products for c-fos,fos-b, c-jun and jun-b were displayed by immunocytochemistry. Areas examined included the ventrolateral septum, hypothalamic paraventricular nucleus, amygdala, locus coeruleus and nucleus of the solitary tract. Acute restraint increased Fos immunoreactivity in all of the areas examined, with the exception of the medial amygdala. The pattern of induction for Fos-B and Jun-B was similar, while c-Jun was only increased in the septum (though constitutive levels were high in most structures compared to the other proteins examined). After 14 days of restraint, immediate-early gene immunostaining was reduced in all of the areas examined, though the extent of adaptation depended on the area and immediate-early gene. In the forebrain, Fos expression adapted in the paraventricular nucleus, amygdala and septum, whereas Fos-B and c-Jun adapted incompletely in the septum. In contrast, Jun-B behaved like Fos. In the brainstem, Fos, Fos-B and Jun-B expression adapted in the nucleus of the solitary tract (but not the locus coeruleus). Corticosterone levels were still raised above baseline, but the response was blunted compared to acute stress. There was marked stress-induced hypothermia which did not adapt during the restraint session, but this returned to baseline during restraint after about five days. In contrast, stress-induced tachycardia did not change during repeated restraint. Dehydroepiandrosterone implants had no clear-cut effects on any immunostaining following acute stress, though there was a trend towards lessened adaptation of the Fos response in the septum after steroid treatment. Dehydroepiandrosterone also did not affect the cardiovascular or endocrine responses to repeated restraint. These experiments show that adaptation of the expression of multiple immediate-early genes occurs during repeated restraint, but in a site-specific pattern in the brains of male rats.
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PMID:Multiple immediate-early gene expression during physiological and endocrine adaptation to repeated stress. 1062 69


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