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)

Two paradigms of acute stress in the rat were used to produce changes in the stomach. The first involved restraint stress combined with water immersion and the second utilized acute intragastric exposure to absolute ethanol. The mRNA expression of immediate early genes (IEG) such as c-fos, c-jun and NGFI-A, cyclooxygenase (COX)-2 and heat shock proteins (HSP) 70 in the stomach were studied using in situ hybridization histochemistry. Upregulation of IEG and HSP70 mRNAs were observed in the smooth muscle cells of muscularis mucosae, muscularis externa and blood vessels in response to water immersion-restraint stress or intragastric application of absolute ethanol. In the restraint stress model, IEG (c-fos and NGFI-A) mRNAs were induced in the pit and isthmus of the mucosa, while in the ethanol exposure model, IEG (c-fos, c-jun and NGFI-A) and HSP70 mRNAs were upregulated in the damaged epithelium, especially surrounding the deep erosions. COX-2 mRNA was detected in surface mucous cells under desquamation. These distinct gene expressions in the mucosa indicate that the two stress paradigms produce different cellular responses. These data provide new insights into cellular mechanisms that occur during the pathogenesis of acute gastric mucosal lesions.
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PMID:Distinct gene expression in the stomach following stress and alcohol exposure. 1172 71

It is well known that stress affects the central nervous system (CNS), neuroendocrinoimmune system and other peripheral organs such as the gastrointestinal tract. However, the process of adaptation or recovery after acute stress reactions in these systems or organs during prolonged stress has not yet been adequately investigated. To clarify the process of adaptation or recovery in these systems and organs after acute stress reactions, the time course of these responses during a single long-duration restraint stress (RTS) was studied. The expression of c-fos in the hypothalamic paraventricular nucleus (PVN) region of the brain was induced and reached a peak at 0.5 hours for c-fos mRNA and 4 hours for c-fos protein (Fos), but disappeared at 2 hours for mRNA and 16 hours for Fos during continuous RTS. The activation of the hypothalamic-pituitary-adrenal (HPA) axis during stress resulted in rapid increases in the plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone (CORT). Whereas the increase in ACTH was transient, the rise in CORT was maintained throughout the duration of the stress. A rapid significant decrease after stress exposure and following a slow and complete or partial recovery were observed in a number of total white blood cells (WBC), lymphocytes (LYM), helper T cells (Th) and cytotoxic/suppressor T cells (CTL/Ts). A gastric ulcer was found in 1/6 and 6/6 rats at 8 hours and 16 hours RTS, respectively. These results suggest that adaptive changes may occur in c-fos expression in the PVN, ACTH release and immune response, but not for CORT release, following acute stress reaction during long-duration RTS. In addition, any associated organic damage, such as gastric ulceration, was also suggested to possibly be progressive according to the duration of RTS.
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PMID:PVN c-fos expression, HPA axis response and immune cell distribution during restraint stress. 1206 82

The bed nuclei of the stria terminalis (BST) and the central nucleus of the amygdala are highly heterogeneous structures, which form one functional unit, the so-called extended amygdala. Several studies described increased c-fos expression following acute stress in this brain area, confirming its central role in the modulation/regulation of stress responses. The oval nucleus of the BST and the central amygdala exhibit a dense network of pituitary adenylate cyclase-activating polypeptide (PACAP)-immunoreactive (ir) fiber terminals. In addition, several dopamine- and cyclic AMP-regulated phosphoprotein (DARPP-32)-immunoreactive neurons were also observed here. Because the extended amygdala plays an important role in the central autonomic regulation during stress and the distribution of PACAP-ir and that of DARPP-32-ir nervous structures overlap, the aims of this study were to investigate the possible activation of DARPP-32-ir neurons following acute systemic stress and to demonstrate synaptic interactions between DARPP-32-ir neurons and fiber terminals immunopositive for PACAP.In summary, this study provided morphological evidence that acute stress resulted in the activation of DARPP-32 neurons, which were innervated by PACAP-ir neuronal structures in the extended amygdala. Furthermore, interaction between neuropeptides/neurotransmitters and phosphoproteins was also demonstrated.
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PMID:Dopamine- and cyclic AMP-regulated phosphoprotein-immunoreactive neurons activated by acute stress are innervated by fiber terminals immunopositive for pituitary adenylate cyclase-activating polypeptide in the extended amygdala in the rat. 1240 16

Besides corticotropin releasing factor, central stress regulatory pathways utilize various neurotransmitters/neuropeptides, such as urocortin and cocaine and amphetamine-regulated transcript, which play an important role in modifying the efferent components of endocrine, immune and behavioral responses to stress. Urocortin's distribution in the rat's brain has been demonstrated, with the most abundant urocortin-ir perikarya present in Edinger-Westphal nucleus. Cocaine and amphetamine-regulated transcript is widely expressed in the rat brain, with a dominant seat of cellular expression also in the Edinger-Westphal nucleus. Since immediate early gene expressions were seen in several midbrain regions, such as in the Edinger-Westphal nucleus, following various acute stresses, the Edinger-Westphal nucleus has been postulated to exert a regulatory/modulatory control over stress responses. Based on these data we decided to investigate the possible colocalization of urocortin and cocaine and amphetamine-regulated transcript-ir in the Edinger-Westphal nucleus using semithin double-label immunofluorescence technique. Furthermore, we also studied whether urocortinergic neurons colocalizing with cocaine and amphetamine-regulated transcript are recruited by lipopolysaccharide stress. Our experiments revealed that urocortin and cocaine and amphetamine-regulated transcript immunoreactivities colocalize in the Edinger-Westphal nucleus. In addition, our studies using the inducible immediate early gene c-fos as a marker of activated neurons demonstrated a significant stress-induced activation in perikarya colocalizing urocortin- and cocaine and amphetamine-regulated transcript-ir in the Edinger-Westphal nucleus. In view of these data it can be postulated that neurons colocalizing cocaine and amphetamine-regulated transcript and urocortin immunoreactivities respond to acute stress, and may play a role in modulating various physiological functions, such as feeding behaviors.
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PMID:Neurons colocalizing urocortin and cocaine and amphetamine-regulated transcript immunoreactivities are induced by acute lipopolysaccharide stress in the Edinger-Westphal nucleus in the rat. 1255 87

We reported previously that acute stress and intracerebroventricular (i.c.v.) injection of corticotropin-releasing factor (CRF) increased neuronal activation and CRF type-1 receptor (CRFR-1) mRNA expression in the CRF-producing neurons of the parvocellular paraventricular nucleus (PVN) of the hypothalamus. In this study, to determine whether CRF can act directly on hypothalamic CRF neurons, thereby increasing CRFR-1 expression, microinjection of CRF into PVN neurons in vivo and primary cultures of dispersed rat fetal hypothalami in vitro were performed. Microinjection of 0.1 microg of CRF into the PVN significantly increased c-fos and CRFR-1 mRNA expression in the CRF-producing parvocellular PVN, 30 min or 180 min after injection, respectively. This effect was blocked by a CRF antagonist, alpha-helical CRF. CRF, when injected into the lateral ventricle at the same dose, increased neither CRFR-1 nor c-fos mRNA levels in the PVN. Primary culture of hypothalamic neurons revealed that CRFR-1 like immunoreactivity was located in CRF-containing neurons, and that the CRFR-1 mRNA level was significantly increased 4 h after incubation with 10(-8) M CRF. These results demonstrate that CRF directly affects hypothalamic neurons to increase CRFR-1 mRNA expression, providing evidence of a direct role for CRF in the regulation of CRFR-1 expression of hypothalamic neurons.
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PMID:Regulation of corticotropin-releasing factor (CRF) type-1 receptor gene expression by CRF in the hypothalamus. 1273 6

In rats, acute stress substantially increases corticotropin-releasing factor (CRF) type 1 receptor (CRFR-1) mRNA expression in the paraventricular nucleus (PVN) and osmotic stimulation induces both CRF and CRFR-1 mRNA in magnocellular PVN and supraoptic nucleus (SON). However, these phenomena have not been analysed in other species. We compared CRF and CRFR-1 expression in rat and mouse hypothalamus. Male C57BL/6 mice and Wistar rats were exposed to acute restraint stress for 3 h, or to hypertonic saline ingestion for 7 days. Restraint stress increased CRF and c-fos mRNA expression in both rat and mouse PVN. CRFR-1 mRNA was barely detectable in controls, whereas restraint stress substantially increased CRFR-1 mRNA in rat PVN, but not in mouse. Hypertonic saline ingestion induced CRF mRNA in magnocellular PVN and SON of the rat, but did not alter CRF mRNA levels in mouse hypothalamus. CRFR-1 mRNA was also induced in magnocellular PVN and SON of the rat in response to osmotic stimulation, but not in mouse. Immunohistochemistry demonstrated that CRFR-1-like immunoreactivity (ir) was distributed within parvocellular and magnocellular PVN of mouse and rat. CRFR-1-ir in rat PVN was increased by acute stress and osmotic stimulation. By contrast, these treatments did not alter CRFR-1-ir in mouse PVN. Combined immunohistochemistry and in situ hybridization revealed that CRFR-1-ir was most frequently colocalized to CRF in mouse PVN, whereas only a small percentage of oxytocin and vasopressin-producing cells coexpressed CRFR-1-ir. These results indicate that (i) by contrast to rats, neither acute stress nor osmotic stimulation induces CRFR-1 mRNA expression in the mouse PVN; (ii) osmotic stimulation does not alter CRF mRNA expression in parvocellular and magnocellular neurones of mouse PVN; and (iii) acute stress increases c-fos and CRF mRNA to a similar degree in mouse and rat PVN. Thus, differences may exist between mouse and rat in the regulation of CRF and CRFR-1 gene expression in hypothalamus following stress and osmotic stimulation.
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PMID:Corticotropin-releasing factor type-1 receptor mRNA is not induced in mouse hypothalamus by either stress or osmotic stimulation. 1296 35

Subjective tinnitus is a phantom sound sensation that does not result from acoustic stimulation and is audible to the affected subject only. Tinnitus-like sensations in animals can be evoked by procedures that also cause tinnitus in humans. In gerbils, we investigated brain activation after systemic application of sodium salicylate or exposure to loud noise, both known to be reliable tinnitus-inductors. Brains were screened for neurons containing the c-fos protein. After salicylate injections, auditory cortex was the only auditory area with consistently increased numbers of immunoreactive neurons compared to controls. Exposure to impulse noise led to prolonged c-fos expression in auditory cortex and dorsal cochlear nucleus. After both manipulations c-fos expression was increased in the amygdala, in thalamic midline, and intralaminar areas, in frontal cortex, as well as in hypothalamic and brainstem regions involved in behavioral and physiological defensive reactions. Activation of these non-auditory areas was attributed to acute stress, to aversive-affective components and autonomous reactions associated with the treatments and a resulting tinnitus. The present findings are in accordance with former results that provided evidence for suppressed activation in auditory midbrain but enhanced activation of the auditory cortex after injecting high doses of salicylate. In addition, our present results provide evidence that acute stress coinciding with a disruption of hearing may evoke activation of the auditory cortex. We interpret these results in favor of our model of central tinnitus generation.
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PMID:Expression of c-fos in auditory and non-auditory brain regions of the gerbil after manipulations that induce tinnitus. 1450 32

Exposure of the rat to restraint results in activation of the hypothalamic-pituitary-adrenal (HPA) axis, a characteristic pattern of c-fos expression in the brain and increased cardiovascular function. These responses adapt with repeated exposure of an individual to the same stress. Corticosterone secretion habituates, and c-fos mRNA expression in the paraventricular nucleus of the hypothalamus (PVN) decreases. The increased expression of corticotropin releasing hormone mRNA in the PVN also becomes less prominent, whereas vasopressin mRNA progressively increases. The neural mechanisms responsible for this adaptation remain obscure. Because of its role in conditioned learning, we have hypothesised that the amygdala might be involved in this adaptive process. Here we show that large neurotoxic lesions of the amygdala in male rats do not prevent acute stress activation of the HPA axis following 30 min restraint, whilst more discrete lesions of the central nucleus actually exacerbate the acute response. Rats with large amygdala lesions demonstrate delayed habituation of corticosterone and c-fos to repeated restraint, an affect not apparent with central nucleus lesions. Furthermore we show that neither type of lesion significantly reduced tachycardiac responses to single or repeated restraint as measured by telemetry. We conclude that the amygdala and the central nucleus are not necessary for HPA and cardiovascular activation in response to stress (though the central nucleus may modulate it), and that adaptation to repeated stress is only modestly dependent upon the amygdala.
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PMID:Does the amygdala modulate adaptation to repeated stress? 1514 69

The stressful quality of an experience, as perceived by rats, is believed to be largely represented by the magnitude of a hypothalamic-pituitary-adrenal (HPA) axis response. The hippocampus may be especially important for assessing the stressfulness of psychological stressors such as novel experience. If such is the case then experience-dependent immediate-early gene expression levels within the hippocampus may parallel relative levels of HPA axis activity. We examined this prospect in rats that were placed in four different novel environments (empty housing tub, circular arena, elevated pedestal or restraint tube). Restraint and pedestal produced the largest magnitude of increased ACTH and corticosterone secretion, arena an intermediate level (Experiment 2) and tub the least magnitude of increase. We saw a very similar experience-dependent pattern of relative Fos protein, c-fos mRNA and zif268 mRNA expression in the paraventricular nucleus of the hypothalamus. However, in hippocampus (and select regions of cortex), immediate-early gene expression was associated with the exploratory potential of the novel experience rather than level of HPA axis activity; pedestal and arena elicited the greatest immediate-early gene expression, tub an intermediate level and restraint the least amount of expression. We conclude that the stressfulness of psychological stressors is not represented by the amount of immediate-early gene induction elicited in hippocampus and cortex, nor does there appear to be a general enhancing or depressive influence of acute stress on immediate-early gene induction in those brain regions.
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PMID:Immediate-early gene induction in hippocampus and cortex as a result of novel experience is not directly related to the stressfulness of that experience. 1619 8

It is well established that estrogens markedly enhance the glucocorticoid response to acute stress in females. However, the precise mechanism responsible for this regulation is poorly understood. Here, we tested whether estrogens enhance the activation of the paraventricular nucleus (PVN) of the hypothalamus by measuring stress-induced c-fos mRNA expression in the PVN of restraint-stressed ovariectomized (OVX) rats treated with physiologically relevant doses of estradiol (E(2)), the major female estrogen. As expected, E(2) enhanced plasma corticosterone responses to restraint in OVX females. However, E(2) markedly attenuated the stress-induced c-fos gene expression in the PVN and inhibited plasma ACTH responses in these animals. Furthermore, E(2)-inhibitory effects were mimicked by progesterone (P) alone or in combination with E(2). Interestingly, the suppressive central effects of both E(2) and P were apparently independent of basal paraventricular corticotropin-releasing hormone (CRH) transcription, since these ovarian steroids did not significantly affect PVN CRH mRNA expression in unstressed rats. These unexpected findings suggested that E(2) promotes glucocorticoid hypersecretion in females by additional peripheral (i.e., adrenal) mechanisms. Indeed, E(2) markedly enhanced plasma corticosterone responses and adrenal corticosterone content in dexamethasone-blocked OVX rats challenged with varying doses of exogenous ACTH. These results suggest that enhanced adrenal sensitive to ACTH is an important physiological mechanism mediating E(2)-related glucocorticoid hypersecretion in stressed females.
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PMID:Estrogen potentiates adrenocortical responses to stress in female rats. 1717 93


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