Showing papers on "Chronic stress published in 1988"
TL;DR: Rising basal corticosterone levels suggest that repeated restraint produced a chronic stress state in these rats which may vary in some qualitative way with stressor intensity, and intraspecific communication of the intensity of stress.
284 citations
TL;DR: It is suggested that chronic restraint leads to compensatory increases of brain 5‐HT and NA synthesis and sensitizes both monoaminergic systems to an additional acute stress and changes may affect coping with stress demands.
Abstract: The effects of 1 h/day restraint in plastic tubes for 24 days on the levels of serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), tryptophan (TP), and noradrenaline (NA) in six regions of rat brain 20 h after the last restraint period were investigated. The levels of 5-HT, 5-HIAA, and NA but not TP increased in several regions. The effects of 1 h of immobilization on both control and chronically restrained rats were also studied. Immobilization per se did not alter brain 5-HT, 5-HIAA, and TP levels, but decreased NA in the pons plus medulla oblongata and hypothalamus. However, immobilization after chronic restraint decreased 5-HT, increased 5-HIAA, and decreased NA in most brain regions in comparison with values for the chronically restrained rats. We suggest that chronic restraint leads to compensatory increases of brain 5-HT and NA synthesis and sensitizes both monoaminergic systems to an additional acute stress. These changes may affect coping with stress demands.
216 citations
TL;DR: The hypothesis that CRF is hypersecreted in patients with major depression, the concentration of CRF in cerebrospinal fluid (CSF) in drug-free depressed patients and age- and sex-matched controles was measured in two studies, and depressed patients exhibited a clear group-related increase in CSF CRF concentrations.
Abstract: It is well established that corticotropin-releasing factor (CRF), a peptide comprised of 41 amino acids, is the major physiological regulator of the pituitary-adrenal axis by virtue of its role as the hypothalamic hypophysiotropic hormone that modulates the secretion of adrenocorticotropin (ACTH) from the anterior pituitary gland. In addition to its neuroendocrine role, CRF appears to function as a neurotransmitter or neuromodulator in extrahypothalamic brain areas. The peptide and its receptors are distributed throughout the central nervous system (CNS), and CRF is released by depolarizing concentrations of potassium in a calcium-dependent manner. After direct CNS administration, CRF produces a number of behavioral and physiological effects that are reminiscent of both an organism's response to stress and to the symptoms of patients with major depression. These include: diminished food consumption, decreased sexual behavior, disturbed sleep, alterations in locomotor activity and sympathetic nervous system activation. Alterations in regional brain CRF concentration in rats were observed after acute and chronic stress, i.e. decreased hypothalamic and increased locus coeruleus CRF concentrations. To test the hypothesis that CRF is hypersecreted in patients with major depression, the concentration of CRF in cerebrospinal fluid (CSF) in drug-free depressed patients and age- and sex-matched controles was measured in two studies. The depressed patients exhibited a clear group-related increase in CSF CRF concentrations. To further test this hypothesis that CRF is chronically hypersecreted in depressed patients, the number and affinity of CRF receptors in frontal cortex was measured in a group of suicides and age-matched controls.(ABSTRACT TRUNCATED AT 250 WORDS)
188 citations
TL;DR: Data indicate that the existence of cross-adaptation to stressors might depend on the variable measured, the central nervous system pathways controlling the pituitary-adrenal axis being, apparently, resistant to cross- Adaptation.
Abstract: The effects of previous chronic immobilization stress on the physiological responses of male rats to a novel chronic stressor (shock) were studied. Previous chronic exposure to immobilization reduced adrenocorticotropin (ACTH) and lactate responses to acute immobilization stress without altering the response to a novel acute stressor (tail shock). When subjected to chronic tail shock, body weight inhibition caused by chronic shock was greater in the rats not previously exposed to chronic immobilization, which suggests that there is cross-adaptation between different stressors. However, adrenocorticotropin adaptation to chronic shock was impaired by previous chronic immobilization. These data indicate that the existence of cross-adaptation to stressors might depend on the variable measured, the central nervous system pathways controlling the pituitary-adrenal axis being, apparently, resistant to cross-adaptation. This lack of cross-adaptation at certain levels can assure the maintenance of an adequate response to unknown environmental stimuli.
130 citations
TL;DR: Several variables appear to influence this pattern of neuroendocrine adaptation to stressful stimulation, including predictability of the stressor, the intensity and duration of the pressure, the interval between each episode of stress, and the number of presentations of the Stressor.
109 citations
TL;DR: Behavioral and endocrine effects in male and female rats treated daily with unpredictable emotional stressor or unpredictable physical stressors over a 14-day period revealed that females were more resistant than males to the behavioral effects of the PS treatment.
79 citations
TL;DR: The initial stress response during chronic stress showed no adaptation but actual sensitization for COR, and repeat stress values of E were the same while those of NE and COR were significantly lower as compared with the last chronic stress value.
61 citations
TL;DR: It would appear that the GABAergic system in the corpus striatum of the rat is most sensitive to acute stress and that theSystem in the frontal cerebral cortex area is preferentially responsive to chronic stress.
Abstract: 1 The function of gamma-aminobutyric acid (GABA)ergic systems in response to acute and repeated stressful manipulations was evaluated in both the corpus striatum and frontal cerebral cortex of the rat 2 In the corpus striatum the activity of the synthetic enzyme for GABA (glutamic acid decarboxylase, GAD) and the levels of GABA were reduced by acute immobilization stress (1 h) GABA turnover was reduced only by acute cold stress (3 h, 4 degrees C) 3 In the frontal cerebral cortex no changes were observed after acute stressful manipulations, but repeated stress (05 h immobilization per day for 14 days) enhanced both GAD activity and GABA turnover, and reduced GABA levels 4 In conclusion, it would appear that the GABAergic system in the corpus striatum of the rat is most sensitive to acute stress and that the system in the frontal cerebral cortex area is preferentially responsive to chronic stress It is speculated that the cortical GABAergic system is responsible for adaptive responses to the adverse conditions prevailing during chronic stress
59 citations
TL;DR: Chronic stressed mice, tested 24 hr after the last stressful experience, showed an increased sensitivity to the inhibitory effects of low doses of apomorphine on climbing behavior and a decreased sensitivity toThe inhibitoryeffects of the same doses of the dopamine agonist on locomotion.
50 citations
TL;DR: It is suggested that chronic but not acute stress reduces the reactivity of α 2 -adrenoceptors involved in clonidine-induced sedation, and a regulatory mechanism of endogenous opioids seems to participate on α 2-adrenOceptors adaptative changes.
Abstract: Low doses of clonidine (50–100 μg/kg IP) evoke a clear dose-dependent hypoactivity response. Seven daily immobilization sessions prevented the motor activity decrease induced by clonidine. On the contrary, a single stress failed to modify clonidine response. Pretreatment with naltrexone (2 mg/kg IP) fully antagonized the attenuating effect induced by chronic stress on clonidine sedative action. These evidences suggest that chronic but not acute stress reduces the reactivity of α 2 -adrenoceptors involved in clonidine-induced sedation. In addition, a regulatory mechanism of endogenous opioids seems to participate on α 2 -adrenoceptors adaptative changes.
46 citations
TL;DR: A complex interaction between pituitary-adrenal responses to stress and changes in natural cytoxicity is suggested.
TL;DR: Experiments indicate that acute and chronic stress activate central muscarinic mechanisms, and these mechanisms may be involved in the patho-physiology of depressive disorders and stress.
TL;DR: Findings suggest that there may be a positive feedback effect of glucocorticoids at the pituitary level under some conditions of chronic stress.
TL;DR: The results suggest that endogenous corticosterone serves to maintain the above escape behavior during chronic stress.
TL;DR: It is concluded that glucose intolerance may play a key role in the altered stress-induced metabolic responses of aged rats and with age, there is a loss of plasticity in physiological adaptive response mechanisms associated with metabolic responses to stress.
Abstract: The effect of age on the capacity of an organism to mobilize glucose and free fatty acids during stress and to adapt these responses from an acute to a chronic stress situation is not known. The purpose of this study was to determine whether aging impaired the capacity to 1) raise glucose and free fatty acid levels and suppress insulin release in acute stress situations and 2) develop adaptation of these responses to exposure to chronic stress. Our results indicate that 6-mo-old rats (young) trained to escape electric shock (short-term modulation) showed greater acute stress-induced hyperglycemic, hypoinsulinemic, and lipolytic responses than untrained young rats. By contrast, in 22-mo-old rats (old), responses of trained and untrained animals were not different. In the chronic stress (long-term adaptation) experiments, it was found that 1) adaptation of stress-induced hyperglycemia occurred at a faster rate in young than in old animals; 2) in young but not in aged rats, a strong positive correlation was observed between adaptation of stress-induced hyperglycemia and hypoinsulinemia; and 3) in young rats, stress-induced lipolytic responses declined proportionately to the duration of chronic stress exposure, whereas by contrast in chronically stressed aged rats steady-state levels of free fatty acids were not raised during exposure to stress. Thus we conclude that 1) glucose intolerance may play a key role in the altered stress-induced metabolic responses of aged rats; 2) with age, there is a loss of plasticity in physiological adaptive response mechanisms associated with metabolic responses to stress.
TL;DR: The results suggest a possible relationship between the development of hypertension and the Hypothalamus-Hypophysis-adrenal (HHA) axis stimulation in rats.
Abstract: We have studied the effect of chronic noise stress (St) and ACTH administration (Ac) affecting blood pressure and plasma corticosterone levels in male Wistar rats. Both chronic treatments elicited an increase in plasma corticosterone and blood pressure levels. The blood pressure increased from the first week of treatment period in St and Ac rats and remained high 4 weeks after the end of the stress period. However, blood pressure elevation decrease progressively during the first three weeks of post-treatment in ACTH administrated rats. The rise of blood pressure levels was due to the effect of chronic treatment. This was demonstrated by the absence of differences between the two values of blood pressure measurement with and without daily treatment in both St and Ac groups. Increased corticosterone levels decreased rapidly during the post-treatment period in St and Ac rats. The results suggest a possible relationship between the development of hypertension and the Hypothalamus-Hypophysis-adrenal (HHA) axis stimulation in rats.
TL;DR: It appears that younger hamsters can maintain reproductive function during stress, but older ones may not be able to do so, and chronic stress produced lower plasma testosterone and testes weights in hamsters with heart failure than in age-matched stressed, healthy hamsters.
Abstract: The effects of old age, chronic disease, and stress on testicular function were examined in Syrian hamsters living on a 12-hr photoperiod. Plasma testosterone concentrations and testes weights were maintained in healthy hamsters 16-19 months of age, but chronic stress decreased plasma testosterone in these old hamsters and not in younger ones (8-11 months of age). Chronic disease in the form of congestive heart failure (CHF) in cardiomyopathic hamsters also decreased plasma testosterone and testes weights, although it is not clear what aspects of this disease affected testicular function. There was an interaction between disease and stress, in that chronic stress produced lower plasma testosterone and testes weights in hamsters with heart failure than in age-matched stressed, healthy hamsters. It appears that younger hamsters can maintain reproductive function during stress, but older ones may not be able to do so. Congestive heart failure in hamsters clearly impairs normal reproductive function by itself; it also makes them more susceptible to stress, so that combining stress and disease results in almost complete suppression of plasma testosterone levels.
Journal Article•
TL;DR: Stress-induced increases in the binding of [3H]CHA to brain membranes from the hypothalamus of rats sacrificed following three days of chronic stress in an around-the-clock intermittent footshock avoidance/escape paradigm are reported.
Abstract: We previously reported an increase in the binding of [3H]cyclohexyladenosine ([3H]CHA) to brain membranes from the hypothalamus of rats sacrificed following three days of chronic stress in an around-the-clock intermittent footshock avoidance/escape paradigm ("sustained performance" stress). Here we report stress-induced increases in [3H]CHA binding to hypothalamic membranes from rats stressed for 14 days in that escape/avoidance paradigm, in rats exposed to repeated restraint (3 hr/day for 10 days) and in rats exposed to four days of "activity-stress." Data from saturation binding experiments indicate that this up-regulation was due to an increase in the apparent number of [3H]CHA binding sites without change in affinity for [3H]CHA. Neither restraint for one three-hr period nor one 15-min exposure to intermittent footshock resulted in significant changes in [3H]CHA binding to hypothalamic membranes. Our present data demonstrate small but consistent increases in the number of [3H]CHA binding sites in hypothalamic membranes from rats stressed in several different chronic stress models but no change by acute stress.
Journal Article•
TL;DR: Chromatographic analysis indicated that acute and chronic stress promoted the accumulation of beta-lipotropin rather than beta-endorphin in the AP, which was attenuated by TP and the only form of immunoreactivity detected in the NIL and hypothalamus.
TL;DR: The subjects were anaesthetists on a cardiothoracic unit and the physiological measures taken were urinary cortisol and salivary flowrate and perceived stress and arousal were monitored using self-report techniques.
Abstract: A distinction is made between acute and chronic stress in the workplace. The distinction leads on to two types of question: (1) How does the one relate to the other? (2) Is it possible to distinguish between acute and chronic stress physiologically? Preliminary attempts to tackle the latter question are reported. The subjects were anaesthetists on a cardiothoracic unit and the physiological measures taken were urinary cortisol and salivary flowrate. Perceived stress and arousal were monitored using self-report techniques. Among the results obtained were the following:
1
Self-reported arousal was higher in the morning than the afternoon.
2
The level of arousal was associated with salivary flow, flow being weaker when arousal was higher and vice versa.
3
Self-reports of stress were associated with higher than average urinary cortisol levels.
4
The mean level of urinary cortisol over 24 hours was significantly higher for the group than that found in the general population.
TL;DR: It is indicated that IR-BE levels in the plasma, the AP, and the NIL of female rats are affected by immobilization stress and that estrogen modulates the effects of acute immobilization Stress onIR-BE Levels in the AP and theNIL and the effects on the levels of IR- BE in the Nil.
Abstract: Immunoreactive beta-endorphin (IR-BE) levels in the plasma, anterior pituitary (AP), the neurointermediate lobe of the pituitary (NIL), and the hypothalamus were determined in castrated female rats and castrated female rats treated with estradiol benzoate (estrogen), after exposure to acute (once for 45 min) or chronic (45 min each day for 15 consecutive days) immobilization stress. Acute and chronic stress increased plasma levels of IR-BE to the same extent in castrated female rats and castrated female rats treated with estrogen. In castrated female rats, acute stress produced an increase in the concentration of IR-BE in the AP, which was attenuated by the administration of estrogen. Although IR-BE in the NIL was not influenced by acute stress in castrated animals, exposure to acute stress resulted in an elevation in IR-BE levels in the NIL of rats given estrogen. Chronic stress did not affect the concentration of IR-BE in the AP of castrated females or castrated females treated with estrogen. Chronic stress did, however, increase the concentration of IR-BE in the NIL of castrated animals. This affect of stress on IR-BE levels in the NIL was potentiated by estrogen administration. IR-BE levels in the hypothalamus were reduced by estrogen and were not affected by acute or chronic stress, regardless of the gonadal steroid environment. As determined by column chromatography, administration of estrogen, as well as subjection to chronic stress, promoted the processing of the proopiomelanocortin precursor to form beta-lipotropin rather than beta-endorphin in the AP. By these methods, the only immunoreactivity detected in the NIL and the hypothalamus was beta-endorphin. These data indicate that IR-BE levels in the plasma, the AP, and the NIL of female rats are affected by immobilization stress and that estrogen modulates the effects of acute immobilization stress on IR-BE levels in the AP and the NIL and the effects of chronic immobilization stress on the levels of IR-BE in the NIL.
TL;DR: Data indicate that previous chronic CMI administration does not prevent changes in the secretory activity of the pituitary-adrenal system or the reduction of food intake and body weight caused by strong stressors.
Abstract: The effects of previous chronic administration of the tricyclic antidepressant drug chlorimipramine (CMI) on some physiological responses of adult male rats to stress has been studied. CMI significantly reduced food intake and body weight gain, but did not alter either adrenal weight or basal serum corticosterone levels. Corticosterone response to 1 h of immobilization stress was the same in saline and CMI-treated rats. When the rats previously treated with CMI were subjected to chronic immobilization stress, it was found that the drug did not alter the anorexic effects of the stressor, but reduced the rate of adaptation of adrenocorticotropin response to stress. These data indicate that previous chronic CMI administration does not prevent changes in the secretory activity of the pituitary-adrenal system or the reduction of food intake and body weight caused by strong stressors.
TL;DR: Treatment of the panic disorder with benzodiazepines does not further lower the UFC levels in patients with uncomplicated panic disorder despite clinical improvement, but it does lower UFC levels into the normal range in those with concurrent depression and agoraphobia.
TL;DR: Adrenal demedullation was effective in attenuating plasma A during stress and reduced the plasma noradrenaline response, and the larger pressor responses of the ADM group seem to result from attenuation of beta-adrenoreceptor-mediated dilation of skeletal muscle vasculature.
Abstract: Because chronic infusions of adrenalin (A) produce hypertension in rats, it has been suggested that A is a mediator of stress-induced hypertension. In order to test the hypothesis that lowering A will attenuate stress-induced hypertension, rats who had their adrenal medullae removed (ADM) and sham-operated controls were subjected to chronic stress. All subjects were offspring of a cross between spontaneously hypertensive and Wistar-Kyoto rats. Prior to chronic stress, systolic pressures were the same in the two groups. The stress consisted of 60 2-h sessions of shock-shock conflict during 18 weeks. After conflict stress, the rats were implanted with arterial catheters and allowed two days to recover. The resting mean arterial pressure (MAP) was 141.2 mmHg in the ADM group and 142.3 mmHg in the Sham group. Cardiovascular responses to acute stress were then examined. The rats were transferred to a test-box and subjected to pulsed foot shocks (0.5-s duration, 5-s intervals) for 5 min. The MAP increase after transfer was 22.3% in the ADM and 4.2% in the Shams (P < 0.001). After termination of the shocks, the MAP was elevated 22.2% above baseline in the ADM and 8.1 % in the Shams (P < 0.02). Five minutes after foot shocks the MAP increase was 21.6% in the ADM and 7.2% in the Shams (P < 0.02). Adrenal demedullation was effective in attenuating plasma A during stress and reduced the plasma noradrenaline response. Therefore, the larger pressor responses of the ADM group seem to result from attenuation of β-adrenoreceptor-mediated dilation of skeletal muscle vasculature. If lowering A has a beneficial effect, it may have been offset by attenuation of β-adrenergic vasodilation.
TL;DR: The role of stress in depressive illness is discussed together with utility of the "learned helplessness" model and some neuropharmacological correlates of uncontrollable shock and the role of adaptive process in stress on antidepressant treatments is discussed.
Abstract: 1. The role of stress in depressive illness is discussed together with utility of the "learned helplessness" model and some neuropharmacological correlates of uncontrollable shock. 2. Similarities and differences between chronic antidepressant treatment and chronic stress treatment regimes are reviewed. 3. Finally the role of adaptive process in stress on antidepressant treatments is discussed.
TL;DR: Results support the hypothesis that this chronic stress model might induce a depressivelike state in the rat and examine the effect of these chronic stress models on the pituitaryadrenal axis, as reflected in growth hormone.
TL;DR: An experiment is reported in which nuclear morphology of adenohypophyseal cells from 49 male rats exposed to a chronic, low‐intensity stressor was examined, and optical density analysis indicated that chromatin was less tightly packed in the experimental animals.
Abstract: Acute, intense sources of "psychogenic" stress clearly modify the structure and function of the hypophysis, and there are concomitant changes in many peripheral physiological systems. Less dramatic sources of stress yield more equivocal results. An experiment is reported in which nuclear morphology of adenohypophyseal cells from 49 male rats exposed to a chronic, low-intensity stressor was examined both by conventional histological and computer-assisted-image-processing methods. The hypothesis tested was that an unequivocal pattern of morphological changes in the nucleus and nuclear chromatin would be revealed by image processing. Rats were killed after living for a year in a relatively low-stress environment, "crowded" in groups of five animals per cage. The control condition was a minimal stress environment of two rats per cage. Results suggested few signs of pathology from peripheral measures of hypophyseal activity, and direct light microscopic examination of the gland revealed no differences between the two groups. Analysis of computer-enhanced images of the pars distalis nuclei from the adenohypophysis, on the other hand, generated findings that were statistically and biologically significant. Nuclear size increased in the stress condition, the number of chromatin and area occupied by the particles increased, and the position of chromatin shifted toward the periphery of the nucleus. Perhaps more important, optical density analysis indicated that chromatin was less tightly packed in the experimental animals. Implications are that chronic, low-intensity stress modulates nuclear structural changes from a dormant to an active state that portend changes in the peripheral systems influenced by the hypophysis.
Journal Article•
TL;DR: The results suggest that the fluctuations of DNA replication may be connected to compensatory mechanisms aimed at adjusting the gastroduodenal mucosa to protracted stress situations.
Abstract: We investigated the effects of acute and chronic stress on the DNA synthesis of the gastroduodenal mucosa of the rat using two different methods of physical stress at various time intervals. Acute stress was produced in the rats being briefly plunged or swimming for two hours (water temperature 37 degrees C). "Sham - transported" rats were used as controls. The results indicate that in the stomach the DNA synthesis was substantially reduced during acute stress in both groups tested (when compared to controls). The DNA synthesis was also reduced in experimental rats after one and two weeks of stress (as compared to day one). By four and eight weeks, the rate of DNA synthesis in the gastric mucosa had significantly increased in the stressed animals. Controls demonstrated significantly lower DNA values following two to eight weeks of stress (as compared to day one). From the outset, the DNA replication values were 2.5 to 3 times higher in the duodenal mucosa than in the gastric mucosa. Following two weeks of stress, the duodenal mucosa of both test groups showed significantly lower DNA values than controls, but significantly higher values after four weeks of stress. By eight weeks, the duodenal mucosa in all rats had reached the same values as that of day one. This was considered a sign of "adaptation to stress" in the duodenal mucosa. The above results suggest that the fluctuations of DNA replication may be connected to compensatory mechanisms aimed at adjusting the gastroduodenal mucosa to protracted stress situations.(ABSTRACT TRUNCATED AT 250 WORDS)
Journal Article•
TL;DR: This work has shown that during the phase of long-lasting adaptation to chronic emotional painful stress three stages have been distinguished on the basis of physiological and neurobiochemical data.
Abstract: During the phase of long-lasting adaptation to chronic emotional painful stress three stages have been distinguished on the basis of physiological and neurobiochemical data. The first stage (1 week of stress)--transition from urgent to long-lasting adaptation--corresponds to labilization of vegetative indices, predominance of fear reactions and suppression of research behaviour in rats, inhibition of lipid peroxidation, activation of superoxide scavenging activity, decrease in cholesterol content in brain lipids. The second stage (2 weeks of stress)--long-lasting adaptation--is characterized by normalization of the behaviour, stabilization of high blood pressure, maximum brain antiradical activity and low level of lipid peroxidation. The third stage (3 weeks of stress)--transition from long-lasting adaptation to exhaustion--is characterized by blood pressure lowering, disturbed regulation of vegetative functions, behavioural hyperactivity in the open field, increased lipid peroxidation and decreased phospholipid content.