The Experts below are selected from a list of 175371 Experts worldwide ranked by ideXlab platform
Cheryl D Conrad - One of the best experts on this subject based on the ideXlab platform.
-
recovery after Chronic Stress within spatial reference and working memory domains correspondence with hippocampal morphology
European Journal of Neuroscience, 2011Co-Authors: Ann N Hoffman, A Krigbaum, J B Ortiz, Agnieszka Mika, Katie M Hutchinson, Heather A Bimontenelson, Cheryl D ConradAbstract:Chronic Stress results in reversible spatial learning impairments in the Morris water maze that correspond with hippocampal CA3 dendritic retraction in male rats. Whether Chronic Stress impacts different types of memory domains, and whether these can similarly recover, is unknown. This study assessed the effects of Chronic Stress with and without a post-Stress delay to evaluate learning and memory deficits within two memory domains, reference and working memory, in the radial arm water maze (RAWM). Three groups of 5-month-old male Sprague-Dawley rats were either not Stressed [control (CON)], or restrained (6 h/day for 21 days) and then tested on the RAWM either on the next day [Stress immediate (STR-IMM)] or following a 21-day delay [Stress delay (STR-DEL)]. Although the groups learned the RAWM task similarly, groups differed in their 24-h retention trial assessment. Specifically, the STR-IMM group made more errors within both the spatial reference and working memory domains, and these deficits corresponded with a reduction in apical branch points and length of hippocampal CA3 dendrites. In contrast, the STR-DEL group showed significantly fewer errors in both the reference and working memory domains than the STR-IMM group. Moreover, the STR-DEL group showed better RAWM performance in the reference memory domain than did the CON group, and this corresponded with restored CA3 dendritic complexity, revealing long-term enhancing actions of Chronic Stress. These results indicate that Chronic Stress-induced spatial working and reference memory impairments, and CA3 dendritic retraction, are reversible, with Chronic Stress having lasting effects that can benefit spatial reference memory, but with these lasting beneficial effects being independent of CA3 dendritic complexity.
-
a critical review of Chronic Stress effects on spatial learning and memory
Progress in Neuro-psychopharmacology & Biological Psychiatry, 2010Co-Authors: Cheryl D ConradAbstract:The purpose of this review is to evaluate the effects of Chronic Stress on hippocampal-dependent function, based primarily upon studies using young, adult male rodents and spatial navigation tasks. Despite this restriction, variability amongst the findings was evident and how or even whether Chronic Stress influenced spatial ability depended upon the type of task, the dependent variable measured and how the task was implemented, the type and duration of the Stressors, housing conditions of the animals that include accessibility to food and cage mates, and duration from the end of the Stress to the start of behavioral assessment. Nonetheless, patterns emerged as follows: For spatial memory, Chronic Stress impairs spatial reference memory and has transient effects on spatial working memory. For spatial learning, however, Chronic Stress effects appear to be task-specific: Chronic Stress impairs spatial learning on appetitively motivated tasks, such as the radial arm maze or holeboard, tasks that evoke relatively mild to low arousal components from fear. But under testing conditions that evoke moderate to strong arousal components from fear, such as during radial arm water maze testing, Chronic Stress appears to have minimal impairing effects or may even facilitate spatial learning. Chronic Stress clearly impacts nearly every brain region and thus, how Chronic Stress alters hippocampal spatial ability likely depends upon the engagement of other brain structures during behavioral training and testing.
-
Chronic Stress and sex differences on the recall of fear conditioning and extinction
Neurobiology of Learning and Memory, 2009Co-Authors: Sarah E Baran, Charles E Armstrong, Danielle C Niren, Jeffery J Hanna, Cheryl D ConradAbstract:Abstract Chronic Stress effects and sex differences were examined on conditioned fear extinction. Male and female Sprague–Dawley rats were Chronically Stressed by restraint (6 h/d/21 d), conditioned to tone and footshock, followed by extinction after 1 h and 24 h delays. Chronic Stress impaired the recall of fear extinction in males, as evidenced by high freezing to tone after the 24 h delay despite exposure to the previous 1 h delay extinction trials, and this effect was not due to ceiling effects from overtraining during conditioning. In contrast, Chronic Stress attenuated the recall of fear conditioning acquisition in females, regardless of exposure to the 1 h extinction exposure. Since freezing to tone was reinstated following unsignalled footshocks, the deficit in the Stressed rats reflected impaired recall rather than impaired consolidation. Sex differences in fear conditioning and extinction were observed in nonStressed controls as well, with control females resisting extinction to tone. Analysis of contextual freezing showed that all groups (control, Stress, male, female) increased freezing immediately after the first tone extinction trial, demonstrating contextual discrimination. These findings show that Chronic Stress and sex interact to influence fear conditioning, with Chronic Stress impairing the recall of delayed fear extinction in males to implicate the medial prefrontal cortex, disrupting the recall of the fear conditioning acquisition in females to implicate the amygdala, and nonStressed controls exhibiting sex differences in fear conditioning and extinction, which may involve the amygdala and/or corticosterone levels.
-
enriched environment prevents Chronic Stress induced spatial learning and memory deficits
Behavioural Brain Research, 2008Co-Authors: Ryan L Wright, Cheryl D ConradAbstract:Chronic Stress impairs spatial memory and alters hippocampal structure, which are changed in the opposite direction following enriched environment (EE). Therefore, this study incorporated these two paradigms to determine whether EE would prevent Chronic Stress from impairing spatial learning and memory. Young adult male rats were housed in EE for 1 week prior to and throughout 3 weeks of daily restraint Stress. On the day after the end of restraint, rats were trained and tested on either a water maze (19 degrees C or 24 degrees C water temperature) or a spatial recognition Y-maze (4-h and 1-min delay between training and testing). Chronically Stressed rats housed in standard conditions showed impaired acquisition on the 19 degrees C version of the water maze and deficits on the 4-h delay version of the Y-maze. Chronically Stressed rats housed in EE, however, showed intact performance on all tasks. All rats showed intact performance on the 24 degrees C version of the water maze and on water maze probe trials for both versions. The results showed that EE in adulthood prevented spatial learning and memory impairment in Chronically Stressed rats, indicating that the context of Stress exposure impacts susceptibility to Chronic Stress-induced cognitive deficits.
-
Chronic Stress enhances ibotenic acid induced damage selectively within the hippocampal ca3 region of male but not female rats
Neuroscience, 2004Co-Authors: Cheryl D Conrad, J L Jackson, L S WiseAbstract:The purpose of this investigation was to assess the ability of the hippocampus to withstand a metabolic challenge following Chronic Stress. An N-methyl-d-aspartate receptor excitotoxin (ibotenic acid, IBO) was infused into the CA3 region of the hippocampus following a period of restraint for 6 h/day/21 days. Following the end of restraint when CA3 dendritic retraction persists (3 to 4 days), rats were infused with IBO (or vehicle) into the CA3 region of the hippocampus. Stressed male rats showed significantly more CA3 damage after IBO infusion relative to controls and the saline-infused side. Moreover, IBO-exacerbation of damage in males was not observed in the CA3 region 3 to 4 days after acute Stress (6 h restraint), nor in the CA1 region after Chronic Stress. Females were also examined and Chronic Stress did not exacerbate IBO damage in the CA3 region. Overall, these results demonstrate that Chronic Stress compromises the ability of the hippocampus to withstand a metabolic challenge days after the Chronic Stress regimen has subsided in male rats. Whether the conditions surrounding CA3 dendritic retraction in females represents vulnerability is less clear and warrants further investigation.
John W Wiley - One of the best experts on this subject based on the ideXlab platform.
-
histone h3k9 methylation regulates Chronic Stress and il 6 induced colon epithelial permeability and visceral pain
Neurogastroenterology and Motility, 2020Co-Authors: John W Wiley, Gen Zheng, Ye Zong, Shengtao Zhu, Shuangsong HongAbstract:Background Chronic Stress is associated with activation of the HPA axis, elevation in pro-inflammatory cytokines, decrease in intestinal epithelial cell tight junction (TJ) proteins, and enhanced visceral pain. It is unknown whether epigenetic regulatory pathways play a role in Chronic Stress-induced intestinal barrier dysfunction and visceral hyperalgesia. Methods Young adult male rats were subjected to water avoidance Stress ± H3K9 methylation inhibitors or siRNAs. Visceral pain response was assessed. Differentiated Caco-2/BBE cells and human colonoids were treated with cortisol or IL-6 ± antagonists. Expression of TJ, IL-6, and H3K9 methylation status at gene promoters was measured. Transepithelial electrical resistance and FITC-dextran permeability were evaluated. Key results Chronic Stress induced IL-6 up-regulation prior to a decrease in TJ proteins in the rat colon. The IL-6 level inversely correlated with occludin expression. Treatment with IL-6 decreased occludin and induced visceral hyperalgesia. Chronic Stress and IL-6 increased H3K9 methylation and decreased transcriptional GR binding to the occludin gene promoter, leading to down-regulation of protein expression and increase in paracellular permeability. Intrarectal administration of a H3K9 methylation antagonist prevented Chronic Stress-induced visceral hyperalgesia in the rat. In a human colonoid model, cortisol decreased occludin expression, which was prevented by the GR antagonist RU486, and IL-6 increased H3K9 methylation and decreased TJ protein levels, which were prevented by inhibitors of H3K9 methylation. Conclusions & inferences Our findings support a novel role for methylation of the repressive histone H3K9 to regulate Chronic Stress, pro-inflammatory cytokine-mediated reduction in colon TJ protein levels, and increase in paracellular permeability and visceral hyperalgesia.
-
Chronic Stress and peripheral pain evidence for distinct region specific changes in visceral and somatosensory pain regulatory pathways
Experimental Neurology, 2015Co-Authors: Gen Zheng, Shuangsong Hong, John M Hayes, John W WileyAbstract:Chronic Stress alters the hypothalamic-pituitary-adrenal (HPA) axis and enhances visceral and somatosensory pain perception. It is unresolved whether Chronic Stress has distinct effects on visceral and somatosensory pain regulatory pathways. Previous studies reported that Stress-induced visceral hyperalgesia is associated with reciprocal alterations of endovanilloid and endocannabinoid pain pathways in DRG neurons innervating the pelvic viscera. In this study, we compared somatosensory and visceral hyperalgesia with respect to differential responses of peripheral pain regulatory pathways in a rat model of Chronic, intermittent Stress. We found that Chronic Stress induced reciprocal changes in the endocannabinoid 2-AG (increased) and endocannabinoid degradation enzymes COX-2 and FAAH (decreased), associated with down-regulation of CB1 and up-regulation of TRPV1 receptors in L6-S2 DRG but not L4-L5 DRG neurons. In contrast, sodium channels Nav1.7 and Nav1.8 were up-regulated in L4-L5 but not L6-S2 DRGs in Stressed rats, which was reproduced in control DRGs treated with corticosterone in vitro. The reciprocal changes of CB1, TRPV1 and sodium channels were cell-specific and observed in the sub-population of nociceptive neurons. Behavioral assessment showed that visceral hyperalgesia persisted, whereas somatosensory hyperalgesia and enhanced expression of Nav1.7 and Nav1.8 sodium channels in L4-L5 DRGs normalized 3 days after completion of the Stress phase. These data indicate that Chronic Stress induces visceral and somatosensory hyperalgesia that involves differential changes in endovanilloid and endocannabinoid pathways, and sodium channels in DRGs innervating the pelvic viscera and lower extremities. These results suggest that Chronic Stress-induced visceral and lower extremity somatosensory hyperalgesia can be treated selectively at different levels of the spinal cord.
-
epigenetic regulation of genes that modulate Chronic Stress induced visceral pain in the peripheral nervous system
Gastroenterology, 2015Co-Authors: Shuangsong Hong, Gen Zheng, John W WileyAbstract:Background & Aims Chronic Stress alters the hypothalamic–pituitary–adrenal axis, increases gut motility, and increases the perception of visceral pain. We investigated whether epigenetic mechanisms regulate Chronic Stress-induced visceral pain in the peripheral nervous systems of rats. Methods Male rats were subjected to 1 hour of water avoidance Stress each day, or given daily subcutaneous injections of corticosterone, for 10 consecutive days. L4–L5 and L6–S2 dorsal root ganglia (DRG) were collected and compared between Stressed and control rats (placed for 1 hour each day in a tank without water). Levels of cannabinoid receptor 1 (CNR1), DNA (cytosine-5-)-methyltransferase 1 (DNMT1), transient receptor potential vanilloid type 1 (TRPV1), and EP300 were knocked down in DRG neurons in situ with small interfering RNAs. We measured DNA methylation and histone acetylation at genes encoding the glucocorticoid receptor (NR3C1), CNR1, and TRPV1. Visceral pain was measured in response to colorectal distention. Results Chronic Stress was associated with increased methylation of the Nr3c1 promoter and reduced expression of this gene in L6–S2, but not L4–L5, DRGs. Stress also was associated with up-regulation in DNMT1-associated methylation of the Cnr1 promoter and down-regulation of glucocorticoid-receptor–mediated expression of CNR1 in L6–S2, but not L4–L5, DRGs. Concurrently, Chronic Stress increased expression of the histone acetyltransferase EP300 and increased histone acetylation at the Trpv1 promoter and expression of the TRPV1 receptor in L6–S2 DRG neurons. Knockdown of DNMT1 and EP300 in L6–S2 DRG neurons of rats reduced DNA methylation and histone acetylation, respectively, and prevented Chronic Stress-induced increases in visceral pain. Conclusions Chronic Stress increases DNA methylation and histone acetylation of genes that regulate visceral pain sensation in the peripheral nervous system of rats. Blocking epigenetic regulatory pathways in specific regions of the spinal cord might be developed to treat patients with Chronic abdominal pain.
Carla Denise Bonan - One of the best experts on this subject based on the ideXlab platform.
-
gender differences in aggression and cortisol levels in zebrafish subjected to unpredictable Chronic Stress
Physiology & Behavior, 2017Co-Authors: Cassiano L Rambo, Ricieri Mocelin, Matheus Marcon, Debora Villanova, Gessi Koakoski, Murilo S De Abreu, Thiago Acosta Oliveira, Leonardo Jose Gil Barcellos, Angelo Luis Stapassoli Piato, Carla Denise BonanAbstract:Chronic Stress may cause physical, behavioral and neuropsychiatric changes, affecting the health condition of an individual. Aggression is a universal behavior with great relevance on human and animal social systems. Despite studies showing the influence of Chronic Stress on aggression, the effects of unpredictable Chronic Stress (UCS) on aggressive behavior in male and female zebrafish remain unknown. Thus, the aim of this study was to evaluate the effects of UCS on the aggressive behavior and cortisol levels in adult zebrafish of both sexes. Our results showed that UCS increased aggression in males, but not in females, which displayed more aggressive behavior at baseline than control males. Increased whole-body cortisol levels were observed in Stressed males; however, no differences were found between female groups. In conclusion, we reported for the first time gender differences on behavioral parameters and cortisol levels in response to UCS in zebrafish. These results highlight the relevance of studying behavioral and physiological parameters in both sexes separately.
-
unpredictable Chronic Stress model in zebrafish danio rerio behavioral and physiological responses
Progress in Neuro-psychopharmacology & Biological Psychiatry, 2011Co-Authors: ângelo L Piato, Leonardo Jose Gil Barcellos, Katiucia Marques Capiotti, Angelica R Tamborski, Jean Pierre Oses, Mauricio Reis Bogo, Diogo R Lara, Monica R M Vianna, Carla Denise BonanAbstract:Zebrafish (Danio rerio) have emerged as a promising model organism to study development, toxicology, pharmacology, and neuroscience, among other areas. Despite the increasing number of studies using zebrafish, behavioral studies with this species are still elementary when compared to rodents. The aim of this study was to develop a model of unpredictable Chronic Stress (UCS) in zebrafish. We evaluated the effects of UCS protocol during 7 or 14 days on behavioral and physiological parameters. The effects of Stress were evaluated in relation to anxiety and exploratory behavior, memory, expression of corticotrophin-releasing factor (CRF) and glucocorticoid receptor (GR), and cortisol levels. As expected, UCS protocol increased the anxiety levels, impaired cognitive function, and increased CRF while decreased GR expression. Moreover, zebrafish submitted to 7 or 14 days of UCS protocol presented increased cortisol levels. The protocol developed here is a complementary model for studying the neurobiology and the effects of Chronic Stress in behavioral and physiological parameters. In addition, this protocol is less time consuming than standard rodent models commonly used to study Chronic Stress. These results confirm UCS in zebrafish as an adequate model to preclinical studies of Stress, although further studies are warranted to determine its predictive validity.
Katrina A Mikofalvy - One of the best experts on this subject based on the ideXlab platform.
-
Chronic Stress alters striosome circuit dynamics leading to aberrant decision making
Cell, 2017Co-Authors: Alexander Friedman, Daigo Homma, Bernard Bloem, Leif G Gibb, Kenichi Amemori, Sebastien Delcasso, Timothy F Truong, Joyce Yang, Adam S Hood, Katrina A MikofalvyAbstract:Summary Effective evaluation of costs and benefits is a core survival capacity that in humans is considered as optimal, "rational" decision-making. This capacity is vulnerable in neuropsychiatric disorders and in the aftermath of Chronic Stress, in which aberrant choices and high-risk behaviors occur. We report that Chronic Stress exposure in rodents produces abnormal evaluation of costs and benefits resembling non-optimal decision-making in which choices of high-cost/high-reward options are sharply increased. Concomitantly, alterations in the task-related spike activity of medial prefrontal neurons correspond with increased activity of their striosome-predominant striatal projection neuron targets and with decreased and delayed striatal fast-firing interneuron activity. These effects of Chronic Stress on prefronto-striatal circuit dynamics could be blocked or be mimicked by selective optogenetic manipulation of these circuits. We suggest that altered excitation-inhibition dynamics of striosome-based circuit function could be an underlying mechanism by which Chronic Stress contributes to disorders characterized by aberrant decision-making under conflict. Video Abstract
Lorenz Deserno - One of the best experts on this subject based on the ideXlab platform.
-
the interaction of acute and Chronic Stress impairs model based behavioral control
Psychoneuroendocrinology, 2015Co-Authors: Christoph Radenbach, Andrea Reiter, Veronika Engert, Zsuzsika Sjoerds, Arno Villringer, Hansjochen Heinze, Lorenz DesernoAbstract:It is suggested that acute Stress shifts behavioral control from goal-directed, model-based toward habitual, model-free strategies. Recent findings indicate that interindividual differences in the cortisol Stress response influence model-based decision-making. Although not yet investigated in humans, animal studies show that Chronic Stress also shifts decision-making toward more habitual behavior. Here, we ask whether acute Stress and individual vulnerability factors, such as Stress reactivity and previous exposure to Stressful life events, impact the balance between model-free and model-based control systems. To test this, 39 male participants (21-30 years old) were exposed to a potent psychosocial Stressor (Trier Social Stress Test) and a control condition in a within-subjects design before they performed a sequential decision-making task which evaluates the balance between the two systems. Physiological and subjective Stress reactivity was assessed before, during, and after acute Stress exposure. By means of computational modeling, we demonstrate that interindividual variability in Stress reactivity predicts impairments in model-based decision-making. Whereas acute psychosocial Stress did not alter model-based behavioral control, we found Chronic and acute Stress to interact in their detrimental effect on decision-making: subjects with high but not low Chronic Stress levels as indicated by Stressful life events exhibited reduced model-based control in response to acute psychosocial Stress. These findings emphasize that Stress reactivity and Chronic Stress play an important role in mediating the relationship between Stress and decision-making. Our results might stimulate new insights into the interplay between Chronic and acute Stress, attenuated model-based control, and the pathogenesis of various psychiatric diseases.