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)

The surgical management of large AVMs (those greater than 6 cm in maximal diameter) should be based on a thorough understanding of the chronic hemodynamic changes produced by lesions and the acute stress placed on the cerebral vasculature by their removal. In addition to haemorrhage, seizure, and headache, these larger lesions often present with symptoms of cerebral vascular insufficiency. Angiography frequently demonstrates a high-flow arteriovenous shunt with evidence of vascular steal from the surrounding brain. In many cases there is a virtual absence of normal hemispheric filling. When the steal is sufficient to produce an area of chronic ischaemia in the brain surrounding the AVM, there is an increased risk of swelling and haemorrhage associated with complete excision. We have developed a strategy for the surgical management of these large lesions that involves a stepwise reduction of flow through the AVM using pre- and intraoperative embolization, followed by complete excision. The details of this management strategy are described, and results in 24 patients with exceptionally large AVMs are presented.
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PMID:Surgical management of large AVMs. 318 23

We studied pronociceptin gene expression following limbic seizures. Northern blot analysis revealed increased pronociceptin mRNA levels in the thalamus (but not in the hippocampus) 3-24 h after kainate administration, with maximal effect (2-fold increase over basal levels) reached at 6 h. No variation in pronociceptin mRNA levels was observed 1-6 h after a stimulus-evoked kindled seizure. Carrageenan failed to affect pronociceptin gene expression in the thalamus, indicating that pain and/or acute stress do not account for kainate effects. In situ hybridization revealed that kainate evokes a dramatic (4-fold) increase in pronociceptin mRNA levels over the thalamic reticular nucleus. Kindled seizures evoked only a small, non-significant increase in pronociceptin gene expression over the dentate gyrus of the hippocampus.
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PMID:Limbic seizures increase pronociceptin mRNA levels in the thalamic reticular nucleus. 1020 86

To elucidate the relationship between stress and seizures, the effect of a single swim stress on the convulsive signs and death produced by several GABA-related and GABA-unrelated convulsants, and the effect of repeated swim stress on picrotoxin-induced convulsions was studied. Mice were subjected to swim stress (10 min swimming at 18-19 degrees C), and the i.v. infusion of convulsants started 15 min thereafter. The latency to the onset of several convulsant signs and death was measured, and the doses of convulsants producing convulsions and death were calculated. Additional experiments included mice swimming at room temperature, and those which were stressed repeatedly (twice a day for four consecutive days, plus one stressful procedure on the fifth day). Swim stress increased the dose needed to produce convulsant signs and death after bicuculline, picrotoxin, pentylenetetrazole, strychnine and 4-aminopyridine, while kainic acid-induced convulsions were not affected. Using picrotoxin infusion, the effect of swimming in room temperature water was less than the effect of swimming in 18-19 degrees C water. In addition, the effect of repeated stress was less than the effect of acute stress on picrotoxin-induced convulsions. The results demonstrate that acute swim stress lowers the convulsive potency of GABA-related and some GABA-unrelated convulsants. Repeatedly stressed animals develop tolerance to anticonvulsive effect of swim stress.
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PMID:Swim stress alters the behavioural response of mice to GABA-related and some GABA-unrelated convulsants. 1116 3

Stress affects seizure susceptibility in animals and humans, but the underlying mechanisms are obscure. Here, we provide evidence that GABA(A) receptor-modulating neurosteroids derived from deoxycorticosterone (DOC) play a role in stress-related changes in seizure control. DOC, an adrenal steroid whose synthesis is enhanced during stress, undergoes sequential metabolic reduction by 5alpha-reductase and 3alpha-hydroxysteroid oxidoreductase to form 5alpha-dihydrodeoxycorticosterone (DHDOC) and allotetrahydrodeoxycorticosterone (THDOC), a GABA(A) receptor-modulating neurosteroid with anticonvulsant properties. Acute swim stress in rats significantly elevated plasma THDOC concentrations and raised the pentylenetetrazol (PTZ) seizure threshold. Small systemic doses of DOC produced comparable increases in THDOC and PTZ seizure threshold. Pretreatment with finasteride, a 5alpha-reductase inhibitor that blocks the conversion of DOC to DHDOC, reversed the antiseizure effects of stress. DOC also elevated plasma THDOC levels and protected mice against PTZ, methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate, picrotoxin, and amygdala-kindled seizures in mice (ED50 values, 84-97 mg/kg). Finasteride reversed the antiseizure activity of DOC (ED50, 7.2 mg/kg); partial antagonism was also obtained with indomethacin (100 mg/kg), an inhibitor of 3alpha-hydroxysteroid oxidoreductase. Finasteride had no effect on seizure protection by DHDOC and THDOC, whereas indomethacin partially reversed DHDOC but not THDOC. DHDOC, like THDOC, potentiated GABA-activated Cl- currents in cultured hippocampal neurons (< or =1 microm) and directly activated GABA(A) receptor currents (> or =1 microm), compatible with a role for DHDOC in the antiseizure activity of DOC. DOC is a mediator of the physiological effects of acute stress that could contribute to stress-induced changes in seizure susceptibility through its conversion to neurosteroids with modulatory actions on GABA(A) receptors including THDOC and possibly also DHDOC.
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PMID:Stress-induced deoxycorticosterone-derived neurosteroids modulate GABA(A) receptor function and seizure susceptibility. 1197 55

The hippocampus is an important structure for declarative, spatial, and contextual memory and is implicated in the perception of chronic pain. The hippocampal formation is vulnerable to damage from seizures, ischemia, and head trauma and is particularly sensitive to the effects of adrenal glucocorticoids secreted during the diurnal rhythm and chronic stress. Adrenal steroids typically have adaptive effects in the short run, but promote pathophysiology when there is either repeated stress or dysregulation of the HPA axis. The damaging actions of glucocorticoids under such conditions have been termed "allostatic load", referring to the cost to the body of adaptation to adverse conditions. Adrenal steroids display both protective and damaging effects in the hippocampus. They biphasically modulate excitability of hippocampal neurons, and high glucocorticoid levels and severe acute stress impair declarative memory in a reversible manner. The hippocampus also displays structural plasticity, involving ongoing neurogenesis of the dentate gyrus, synaptogenesis under control of estrogens in the CA1 region, and dendritic remodeling caused by repeated stress or elevated levels of exogenous glucocorticoids in the CA3 region. In all three forms of structural plasticity, excitatory amino acids participate along with circulating steroid hormones. Glucocorticoids and stressors suppress neurogenesis in the dentate gyrus. They also potentiate the damage produced by ischemia and seizures. Moreover, the aging rat hippocampus displays elevated and prolonged levels of excitatory amino acids released during acute stress. Our working hypothesis is that structural plasticity in response to repeated stress starts out as an adaptive and protective response, but ends up as damage if the imbalance in the regulation of the key mediators is not resolved. It is likely that morphological rearrangements in the hippocampus brought on by various types of allostatic load alter the manner in which the hippocampus participates in memory functions and it is conceivable that these may also have a role in chronic pain perception.
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PMID:Plasticity of the hippocampus: adaptation to chronic stress and allostatic load. 1200 27

Psychosis caused by phencyclidine (PCP) stimulated interest in characterizing rodent behaviors elicited by PCP and its analogues. We have shown that MK-801 antagonizes electrically precipitated seizures (defined as tonic hindlimb extension) and elicits episodes of intense jumping behavior, referred to as "popping," in mice. Moreover, 24 h after stress, MK-801's ability to antagonize electrically precipitated seizures is reduced in outbred NIH Swiss mice. Inbred BALBc mice are more resistant to electrically precipitated seizures than the NIH Swiss strain, and are more sensitive to both MK-801's anticonvulsant effect and ability to elicit popping. In the current experiments, we examined the influence of stress and genetic mouse strain on both MK-801's ability to antagonize electrically precipitated seizures and elicit popping. Stress significantly reduced the threshold voltage for precipitation of seizures in BALBc mice and the anticonvulsant properties of MK-801 in both strains. These data show that factors relevant to schizophrenia and its exacerbation (i.e., acute stress and genetics) influence N-methyl-D-aspartic acid (NMDA) receptor-mediated neurotransmission in intact mice. The BALBc inbred strain of mouse may possess advantages in preclinical screening paradigms designed to assess NMDA receptor agonist interventions for disorders such as schizophrenia. Specifically, stressed BALBc mice showed the greatest behavioral sensitivity to MK-801 with regard to electrically precipitated seizures in the incremental electroconvulsive shock (IECS) paradigm, whereas unstressed BALBc showed the greatest behavioral sensitivity to MK-801 in the "popping" paradigm, relative to BALBc and NIH Swiss mice in the appropriate comparison conditions.
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PMID:Interaction of stress and strain on glutamatergic neurotransmission: relevance to schizophrenia. 1247 54

Recent evidence suggest that endogenous cholecystokinin (CCK) has important roles in central responses to stress. CCK receptors are known as functional modulators of opioidergic system with a tonic antiopioid effect in nociceptive pathways. In contrast, CCK receptor ligands are known to induce anticonvulsant effects similar to endogenous opioids. It is not clear whether endogenous CCK may play a role in the anticonvulsant effects of stress, especially in those stressful paradigms that are associated with strong activation of opioid pathways. The present study examined the role of endogenous CCK receptors in acute stress-induced modulation of seizure (clonic seizures induced by pentylenetetrazole) and nociception (tail-flick) thresholds. Acute restraint stress (for 2 h) and prolonged intermittent footshock stress (30 min) both induced opioid-dependent anticonvulsant and antinociceptive effects. While CCK receptor antagonist proglumide (10, 20, or 40 mg/kg) had no effect on seizure or nociception threshold by itself, it inhibited the anticonvulsant effects of both these types of stress while potentiating their antinociceptive effects. Moreover, proglumide exerted a similar inhibition of the anticonvulsant effect and potentiation of the antinociceptive effect of acute morphine at 1 mg/kg. In contrast, brief and continuous footshock stress (3 min) that induced a nonopioid type of antinociception did not increase the seizure threshold. Proglumide pretreatment did not alter any of these effects of brief footshock stress paradigm. The present data suggest that CCK receptors specifically and differentially modulate the opioid-mediated anticonvulsant and antinociceptive effects of acute stress.
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PMID:Differential contribution of cholecystokinin receptors to stress-induced modulation of seizure and nociception thresholds in mice. 1521 60

Social stress is a common occurrence in our society that can negatively impact health. Therefore, we wanted to study the effects of a mild stressor designed to model social stress on seizure susceptibility and GABAA receptors in male and female rats. The mild chronic stress of individual housing consistently decreased bicuculline (but not pentylenetetrazol, PTZ) seizure thresholds by 10-15% in both sexes. Housing conditions did not alter the anticonvulsant activity of diazepam or ethanol, although the anticonvulsant effect of ethanol was significantly greater against PTZ-induced seizures. Experiments testing the addition of an acute restraint stress unmasked sex differences in seizure induction. The acute stress also selectively decreased the potency of GABA to modulate GABAA receptor-mediated chloride uptake in group-housed females. There were additional sex differences by housing condition for GABAA receptor-gated chloride uptake but no differences in [3H]flunitrazepam binding. We also found significant effects of sex and housing on ethanol-induced increases in corticosterone (CORT) levels. In summary, there were complex and sex-selective effects of mild chronic stress on seizure induction and GABAA receptors. Gaining a better understanding of mechanisms underlying interactions between sex and stress has important implications for addressing health concerns about stress in men and women.
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PMID:Sex differences in effects of mild chronic stress on seizure risk and GABAA receptors in rats. 1525 Dec 58

Stress increases plasma and brain concentrations of corticosteroids and neuroactive steroids. Cortisol is the most important stress hormone in the hypothalamic pituitary adrenocortical system. However, significant amounts of the mineralocorticoid deoxycorticosterone are also released during stress. Deoxycorticosterone undergoes biotransformation to allotetrahydrodeoxycorticosterone, a neuroactive steroid with anxiolytic and anticonvulsant properties. Our studies indicate that the anticonvulsant activity of deoxycorticosterone is mediated by its conversion to allotetrahydrodeoxycorticosterone, which is a potent positive allosteric modulator of GABA(A) receptors. Although the role of allotetrahydrodeoxycorticosterone within the brain is undefined, recent studies indicate that stress induces increases in allotetrahydrodeoxycorticosterone to levels that can activate GABA(A) receptors. These results might have significant implications for human stress-sensitive conditions such as epilepsy, panic disorder, post-traumatic stress disorder, and major depression. In epilepsy, a role for adrenal allotetrahydrodeoxycorticosterone in seizure susceptibility has been suggested. Recent preclinical studies indicate a role of neuroactive steroids in ethanol actions. Although these studies provide a better understanding of the role of allotetrahydrodeoxycorticosterone and related neuroactive steroids in acute stress, further studies are clearly warranted to ascertain the specific role of neuroactive steroids in the pathophysiology of chronic stress and related brain conditions.
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PMID:Physiological role of adrenal deoxycorticosterone-derived neuroactive steroids in stress-sensitive conditions. 1632 48

Human studies show a link between stress and epilepsy, with stress causing an increase in seizure frequency and severity in patients with epilepsy. Many different animal model systems have been used to better understand this connection and the possible mechanisms involved. This review highlights the results of such studies relating stress and seizure susceptibility, with a focus on the hypothalamic-pituitary-adrenal axis and its relationship to seizure generation. The effects of hypothalamic-pituitary-adrenal axis mediators, acute stress, chronic stress, and early life stress on the seizure phenotype are summarized. Results suggest that stress has both anticonvulsive and proconvulsive properties, depending on the animal strain and the stress/seizure induction paradigm used. Attempts to interpret the stress-epilepsy literature must take these variables into account. The growing availability of genetically modified mice that carry either human epilepsy mutations or mutations in stress pathway genes now provide the opportunity to examine the relationship between stress and epilepsy more directly.
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PMID:Stress and epilepsy: multiple models, multiple outcomes. 2107 37


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