Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used in-situ hybridization to study the effect of acute stress on induction of the immediate early genes (IEGs), c-fos and zif/268, in the rat brain. After one hour of restraint plus intermittent tail shock, messenger RNA (mRNA) levels for both genes were significantly increased bilaterally in the neocortex, particularly in layers IV, V and VI, and in the CA1 region of the hippocampus. This regionally-specific response suggests that IEGs may have a role in the mediation of acute stress responses in the central nervous system.
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PMID:Activation of immediate early genes after acute stress. 176 44

The effect of immobilization stress on the expression of c-fos protein in the adrenal cortex of adult rats was investigated immunocytochemically. After immobilization stress lasting for longer than 30 min, an enhanced c-fos-like immunoreactivity was observed in the cortical cells of the zona fasciculata and zona reticulata. Compared to unstressed controls, an about 5-fold increase in the density of the immunoreactive cells in a unit of the cortical area was seen following a 1-h immobilization. The enhanced immunoreactivity lasted for at least 3 h after 1-h immobilization and it began to diminish 5 h after the stress. Furthermore, administration of dexamethasone 2 h prior to 1-h immobilization attenuated the stress-enhanced immunostaining for the c-fos-like protein. These results suggest that an acute stress may cause a dramatic and long-persisting induction of c-fos-like protein in the cortical cells of rat adrenals. The characteristic zonal distribution of the c-fos induction in rat adrenals as well as the effect of dexamethasone suggest involvement of the pituitary adrenocorticotropic hormone (ACTH) in the induction.
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PMID:Induction of c-fos-like protein in the rat adrenal cortex by acute stress--immunocytochemical evidence. 255 26

Centrally administered corticotropin-releasing factor (CRF) produces a number of physiological and behavioral changes akin to those elicited by exposure to acute stress. However, the specific brain site of action responsible for the centrally activating property of CRF has not been precisely determined. In this study, we used in situ hybridization histochemistry for c-fos mRNA to map potential neuronal structures activated after intracerebroventricular (i.c.v.) injection of CRF and compared the distribution of c-fos mRNA with that after stress. Wistar male rats were sacrificed 30, 60, 120 and 180 min after the i.c.v. injection of 1 microgram ovine CRF or vehicle alone. Another group of rats was exposed to immobilization stress for 60 min or electrical foot-shock stress (1.5 mA, 1-s duration, 30 x) for 15 min and sacrificed before and 30, 60, 120 and 180 min after the beginning of stress. Centrally administered CRF rapidly (30-60 min) induced c-fos mRNA expression in most of the areas that showed hybridization signals for c-fos after stress: the limbic structures, including the piriform cortex, cingulate cortex, the lateral septal nucleus, the hippocampus, the anterior corticomedial and the medial amygdaloid nuclei, the hypothalamic nuclei, such as the paraventricular nucleus, the supraoptic nucleus (SO) and the dorsomedial nucleus (DMD), and some brainstem nuclei like the pontine nucleus, the locus ceruleus (LC) and Barrington's nucleus. The granular layer of the cerebellum, some thalamic nuclei and the habenula also showed hybridization signals after i.c.v. injection of CRF and stress. However, c-fos induction in the bed nucleus of the stria terminalis, the central nucleus of the amygdala (CeA) and the nucleus tractus solitarius (SOL) was seen only after i.c.v. administration of CRF; in the septo-hypothalamic nucleus and the superior olive, however, c-fos mRNA expression was observed only after stress. There were no differences in the pattern of c-fos mRNA expression between the two stress paradigms. In contrast, i.c.v. injection of saline-induced expression of c-fos mRNA in the piriform cortex, neocortex, cingulate cortex and the amygdala was much less than that seen after i.c.v.-administered CRF as evident in the intensity of the signals. These results suggest that CRF produces c-fos mRNA expression in the brain areas related to stress response, and that CRF may induce behavioral and neuroendocrine responses through activating these brain structures, such as the limbic system and the hypothalamic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intracerebroventricular administration of corticotropin-releasing factor induces c-fos mRNA expression in brain regions related to stress responses: comparison with pattern of c-fos mRNA induction after stress. 835 2

One important promoter element at the 5' end of the c-fos gene is the serum response element (SRE). SRE is the site of attachment of the 67-kDa protein serum response factor (SRF) and several accessory proteins (Elk1, SAP1, SAP2/NET), termed the ternary complex factors. The binding of SRF to SRE plays an integral role in c-fos transcription and may occur independently of the association of the ternary complex factors. In the current study, we found that SRF protein expression was increased in the hearts of the old vs young adult rats in the basal condition. The hearts of old rats may have posttranslationally modified SRF proteins that are different compared to that of the young adults. The SRF increase was present both in the cytoplasm as well as in the nucleus in the old hearts. To test whether SRF protein levels in response to acute stress might be altered with age, we studied hearts of young adult and old rats during myocardial infarction. The young adult rat hearts responded to acute ischemic stress with an increase in both p62 and p67 SRF. The hearts of the old rats, however, did not exhibit a significant change in SRF protein expression. These findings demonstrate qualitative as well as quantitative age differences in SRF protein levels, both at baseline and following stimulation. The reduced SRF expression in response to acute cardiac ischemic stress in the old rats might contribute to the observed age-related decrease in the induction of immediate early genes such as c-fos in the heart.
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PMID:SRF binding to SRE in the rat heart: influence of age. 946 16

The purpose of this study was to compare the effect of an acute versus a chronic immobilization stress on the genetic expression of c-fos and corticotropin-releasing factor type 1 receptor (CRF1 receptor) in the paraventricular nucleus (PVN) of the rat hypothalamus. Male Sprague-Dawley rats were exposed to either a single 90-min immobilization stress or the same session for 11 consecutive days. Animals were deeply anesthetized before (control); immediately, 1.5, 3, 6, or 12 h after the acute stress; or after the last session of the repeated exposures to immobilization. Coronal frozen sections (30 micrometers) of the brains were cut and mRNAs encoding the rat c-fos and CRF1 receptor were assayed by in situ hybridization histochemistry using 35S-labeled riboprobes. Localization of these transcripts within PVN CRF-immunoreactive (ir) neurons was also determined. The expression of the mRNA encoding either c-fos or CRF1 receptor was barely detectable to low in the PVN of control animals, but the acute stress session induced a robust signal for both transcripts in this endocrine nucleus. Numerous CRF-ir neurons were positive for the gene encoding either c-fos or CRF1 receptor in the PVN of acutely stressed animals. In contrast, the PVN of chronically stressed animals displayed a significantly lower CRF1 receptor mRNA signal after the last stress session. In these animals, stress-induced transcription of c-fos mRNA occurred in the magnocellular PVN 90 min after the end of the last stress session but only a low signal was detected in the parvocellular division. Moreover, very few CRF-ir neurons of the PVN expressed either the CRF1 receptor or c-fos transcript in chronically stressed rats. These data provide evidence for an adaptive cellular mechanism involving an attenuated action of CRF within the PVN in response to repeated homotypic stress exposures.
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PMID:Effect of a chronic stress on CRF neuronal activity and expression of its type 1 receptor in the rat brain. 979 Oct 59

Increased c-fos mRNA or fos immunoreactivity within the central nervous system has been used as a marker of neuronal activation. Acute stress and acute immune challenge result in an increase in c-fos mRNA in corticotrophin-releasing factor (CRF)-containing neurons in the paraventricular nucleus (PVN). It has often been implied that an increase in fos in the PVN can be equated to an increase in the activity of CRF itself, although there is some evidence to suggest these events are not linked. In the present study we have used the rat model of adjuvant-induced arthritis (AA), in which, despite the activation of the pituitary-adrenal system associated with inflammation, there is a paradoxical decrease in CRF mRNA and CRF peptide release. AA rats are unable to mount a hypothalamo-pituitary-adrenal (HPA) axis response to acute stress. They are, however, able to mount a response to acute immune stimulation, e.g. lipopolysaccharide injection. Despite the lack of HPA axis response to stress, there is an increase in c-fos mRNA to these challenges in AA. This suggests that the increase in c-fos mRNA in response to acute stress is not related to a subsequent increase in CRF mRNA in this model. We can conclude that under these conditions, c-fos mRNA is not a good marker of HPA axis activation and independent estimation of the involvement of CRF in the stimulation of the HPA axis should always be obtained. The AA model may prove useful for the comparison of the relationship between immediate early genes and heteronuclear RNAs in response to acute stress and immune stimuli with which to tease apart the molecular mechanisms underlying the control of releasing factor activation at the level of the PVN.
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PMID:Dissociation between c-fos mRNA in the paraventricular nucleus and corticosterone secretion in rats with adjuvant-induced arthritis. 1049 12

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

The precise mechanisms by which beneficial responses to acute stress are transformed into long-term pathological effects of chronic stress are largely unknown. Western blot analyses revealed that members of the AP1 transcription factor family are differentially regulated by single and repeated stress in the rat adrenal medulla, suggesting distinct roles in establishing stress-induced patterns of gene expression in this tissue. The induction of c-fos was transient, whereas marked elevation of long-lasting Fos-related antigens, including Fra2, was observed after repeated immobilization. We investigated DNA protein interactions at the AP1-like promoter elements of two stress-responsive genes, tyrosine hydroxylase and dopamine beta-hydroxylase. Increased DNA-binding activity was displayed in adrenomedullary extract from repeatedly stressed rats, which was predominantly composed of c-Jun- and Fra2-containing dimers. The induction of Fra2 and increased AP1-like binding activity was reflected in sustained transcriptional activation of tyrosine hydroxylase and dopamine beta-hydroxylase genes after repeated episodes of stress. The functional link between Fra2 and regulation of tyrosine hydroxylase and dopamine beta-hydroxylase transcription was confirmed in PC12 cells coexpressing this factor and the corresponding promoter-reporter gene constructs. These studies emphasize the potential importance of stress-evoked increases in the expression of the Fra2 gene for in vivo adaptations of the adrenal catecholamine producing system.
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PMID:Fos-related antigen 2: potential mediator of the transcriptional activation in rat adrenal medulla evoked by repeated immobilization stress. 1090 2

Brainstem noradrenergic neurons, particularly the locus-coeruleus (LC), play a pivotal role in modulating the central stress response and have been implicated in regulating the hypothalamic-pituitary-adrenal (HPA) axis. In adult rats, acute stress causes an increase in LC firing and tyrosine hydroxylase (TH) gene expression. While the role of the LC-norepinephrine (LC-NE) system in the adult stress response has been well characterized, there is limited evidence for its participation during development. Previous studies described the neonatal HPA axis as hyporeactive because of stimulus-selective pituitary activation. However, maternal deprivation does reinstate stress-induced endocrine activity and can amplify the neural stress response. Considering that LC neurons can modulate neuroendocrine activity, we hypothesized that the LC-NE system would be stress-responsive during development. Because maternal deprivation (DEP) can alter the central stress response, we examined the LC-NE stress response in both DEP and non-deprived (NDEP) pups. Following an isotonic saline injection (stressor) the time course of TH, c-fos and glucocorticoid receptor (GR) mRNA was examined. Stress-induced TH mRNA was increased in DEP pups at postnatal day (pnd) 12 and in both NDEP and DEP pups at pnd 18. At 15, 30 and 240 min c-fos mRNA was markedly increased in all groups examined. GR mRNA was not altered at pnd 12; however, at pnd 18 NDEP pups showed reduced GR mRNA expression. These data indicate that during ontogeny the LC-NE system is stress-responsive to an acute mild challenge. Activation of LC-NE neurons suggests that this system may participate in modulating the neuroendocrine stress response during development.
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PMID:Stress-induced alterations in locus coeruleus gene expression during ontogeny. 1128 61

We have previously proposed the existence of ultrashort loop-positive feedback regulation of corticotropin-releasing hormone (CRH) in the hypothalamus. To gain a better understanding of this effect, we performed double-label in situ hybridization to identify the neurons in the paraventricular nucleus (PVN) that express CRH type 1 receptor (CRH-R1) following stress. We also conducted immunohistochemistry to determine whether CRH-R1 mRNA was translated to CRH-R1 protein in the PVN. Thirty-minute restraint stress given to male Wistar rats increased c-fos mRNA expression primarily in the CRH-producing neurons of the parvocellular PVN. Small numbers of vasopressin and oxytoxin-producing cells were also labeled by c-fos probes. Approximately 70% of CRH-R1 positive neurons exhibited CRH mRNA 2 h after the beginning of stress, while only a small percentage of the vasopressin and oxytocin-producing cells coexpressed CRH-R1 mRNA. CRH-R1 immunoreactivity, which was detected in the perikarya and fibers of PVN neurons, appeared to increase in response to stress, though this was not statistically significant. Pretreatment with a selective CRH-R1 antagonist, CP-154,526, significantly attenuated stress-induced corticotropin (ACTH) secretion as well as c-fos mRNA expression in the PVN. These results demonstrate that acute stress increases neuronal activation and CRH-R1 mRNA expression primarily in CRH-producing neurons of the parvocellular PVN, that CRH-R1 message is translated to CRH-R1 protein, and that PVN neurons are activated at least in part through CRH-R1 under acute stress. The data further support the possibility of feedback regulation of CRH itself in CRH-producing neurons.
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PMID:Expression of corticotropin-releasing hormone type 1 receptor in paraventricular nucleus after acute stress. 1139 2


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