Effect of repeated corticosterone injections and restraint stress on anxiety and depression-like behavior in male rats

Gregus, Andrea; Wintink, Amanda J.; Davis, Alicia C; Kalynchuk, Lisa E.

doi:10.1016/j.bbr.2004.05.013

Cited by 370 publications

(251 citation statements)

References 60 publications

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“…Reduction in novel-setting exploration by rats following exposure to stressors is a commonly used and pharmacologically validated index for heightened anxiety, which is highly correlated with other accepted behavioral and physiological anxiety indices (Kalynchuk et al, 1997;Ramos and Mormede, 1998;Campbell et al, 2003;Gregus et al, 2005).…”

Section: Exposure To Stress During Juvenility Alters Emotional Responmentioning

confidence: 99%

Exposure to Stressors during Juvenility Disrupts Development-Related Alterations in the PSA-NCAM to NCAM Expression Ratio: Potential Relevance for Mood and Anxiety Disorders

Tsoory

Guterman

Richter‐Levin

2007

Neuropsychopharmacol

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Childhood trauma is associated with higher rates of both mood and anxiety disorders in adulthood. The exposure of rats to stressors during juvenility has comparable effects, and was suggested as a model of induced predisposition for these disorders. The neural cell adhesion molecule (NCAM) and its polysialylated form PSA-NCAM are critically involved in neural development, activity-dependent synaptic plasticity, and learning processes. We examined the effects of exposure to stressors during juvenility on coping with stressors in adulthood and on NCAM and PSA-NCAM expression within the rat limbic system both soon after the exposure and in adulthood. Exposure to stressors during juvenility reduced novel-setting exploration and impaired two-way shuttle avoidance learning in adulthood. Among naive rats, a development-related decrease of about 50% was evident in the PSA-NCAM to NCAM expression ratio in the basolateral amygdala, in the CA1 and dentate gyrus regions of the hippocampus, and in the entorhinal cortex. In juvenile-stressed rats, we found no such decrease, but rather an increase in the polysialylation of NCAM (B50%), evident soon after the exposure to juvenile stress and also in adulthood. Our results suggest that exposure to stressors during juvenility alters the maturation of the limbic system, and potentially underlies the predisposition to exhibit stress-related symptoms in adulthood.

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Section: Exposure To Stress During Juvenility Alters Emotional Responmentioning

confidence: 99%

Exposure to Stressors during Juvenility Disrupts Development-Related Alterations in the PSA-NCAM to NCAM Expression Ratio: Potential Relevance for Mood and Anxiety Disorders

Tsoory

Guterman

Richter‐Levin

2007

Neuropsychopharmacol

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“…For example, several antidepressant treatments increase neurogenesis Santarelli et al, 2003;Warner-Schmidt and Duman, 2006), although stress, which is widely thought to precipitate depression, reduces neurogenesis (Cameron and Gould, 1994;Gregus et al, 2005;Malberg and Duman, 2003;Tanapat et al, 2001). In addition to stress, alcohol has been shown to reduce neurogenesis.…”

Section: Introductionmentioning

confidence: 99%

Abstinence following Alcohol Drinking Produces Depression-Like Behavior and Reduced Hippocampal Neurogenesis in Mice

Stevenson

Schroeder

Nixon

et al. 2008

Neuropsychopharmacol

131

102

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Alcoholism and depression show high degrees of comorbidity. Clinical evidence also indicates that depression that emerges during abstinence from chronic alcohol use has a greater negative impact on relapse than pre-existing depression. Although no single neurobiological mechanism can account for the behavioral pathologies associated with these devastating disorders, converging evidence suggests that aspects of both alcoholism and depression are linked to reductions in hippocampal neurogenesis. Here, we report results from a novel preclinical behavioral model showing that abstinence from voluntary alcohol drinking leads to the emergence of depressionlike behavior and reductions in neurogenesis. C57BL/6J mice were allowed to self-administer ethanol (10% v/v) vs H 2 O in the home cage for 28 days. Alcohol was then removed for 1 or 14 days, and mice were tested in the forced swim test to measure depression-like behavior. After 14 days, but not 1 day of abstinence from alcohol drinking, mice showed a significant increase in depression-like behavior. The significant increase in depression-like behavior during abstinence was associated with a reduction in proliferating cell nuclear antigen (PCNA) and doublecortin (DCX) immunoreactivity in the dentate gyrus of the hippocampus indicating that both the number of proliferating neural progenitor cells (NPC) and immature neurons were reduced, respectively. The number of NPCs that were labeled with bromo-deoxyuridine (BrdU) at the beginning of alcohol exposure was not altered indicating that survival of NPCs is not linked to abstinence-induced depression. Chronic treatment (14 days) with the antidepressant desipramine during abstinence prevented both the emergence of depression-like behavior and the reduction in hippocampal neurogenesis indicating that abstinence-induced depression is associated with structural plasticity in the hippocampus. Overall, the results of this study support the conclusion that profound functional (ie behavioral) and structural changes occur during abstinence from alcohol use and suggest that antidepressant treatment may alleviate some of these pathological neurobehavioral adaptations.

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“…Previous reports on the effects of repeated restraint on anxiety-related behavior have yielded mixed results. For example, repeated restraint ranging from 10-21 days had no effect on anxiety-related behavior 2 hours later in the EPM (Thorsell et al, 1999;Chadda & Devaud, 2005), or 24 hours later in the open field test (Perrot-Sinal et al, 2004;Gregus et al, 2005) or the social interaction test (Gregus et al, 2005) compared to unstressed controls. However, another study that exposed rats to 14 days of restraint (2 or 8 hours/day) reported a significant decrease in the percentage of time spent in the open arms and number of open arm entries in the EPM compared to unstressed groups 48 hours following the last stress exposure (Kim & Han, 2006).…”

Section: Discussionmentioning

confidence: 92%

Corticotropin-releasing hormone receptors in the medial prefrontal cortex regulate hypothalamic–pituitary–adrenal activity and anxiety-related behavior regardless of prior stress experience

Jaferi

Bhatnagar

2007

Brain Research

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The hypothalamic-pituitary-adrenal (HPA) axis habituates, or gradually decreases its activity, with repeated exposure to the same stressor. During habituation, the HPA axis likely requires input from cortical and limbic regions involved in processing of cognitive information that is important in coping to stress. Brain regions such as the medial prefrontal cortex (mPFC) are recognized as important in mediating these processes. The mPFC modulates stress-related behavior and some evidence suggests that the mPFC regulates acute and repeated stress-induced HPA responses. Interestingly, corticotropin releasing hormone(CRH)-1 receptors, which integrate neuroendocrine, behavioral and autonomic responses to stress, are localized in the mPFC but have not been specifically examined with respect to HPA regulation. We hypothesized that CRH receptor activity in the mPFC contributes to stress-induced regulation of HPA activity and anxiety-related behavior, and that CRH release in the mPFC may differentially regulate HPA responses in acutely-compared to repeatedly-stressed animals. In the present experiments, we found that blockade of CRH receptors in the mPFC with the non-selective receptor antagonist, D-Phe-CRH (50ng or 100ng) significantly inhibited HPA responses compared to vehicle regardless of whether animals were exposed to a single, acute 30min restraint or to the eighth 30min restraint. We also found that intra-mPFC injections of CRH (20ng) significantly increased anxiety-related behavior in the elevated plus maze in both acutely-and repeatedly-restrained groups compared to vehicle. Together, these results suggest an excitatory influence of CRH in the mPFC on stress-induced HPA activity and anxiety-related behavior regardless of prior stress experience.

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Effect of repeated corticosterone injections and restraint stress on anxiety and depression-like behavior in male rats

Cited by 370 publications

References 60 publications

Exposure to Stressors during Juvenility Disrupts Development-Related Alterations in the PSA-NCAM to NCAM Expression Ratio: Potential Relevance for Mood and Anxiety Disorders

Exposure to Stressors during Juvenility Disrupts Development-Related Alterations in the PSA-NCAM to NCAM Expression Ratio: Potential Relevance for Mood and Anxiety Disorders

Abstinence following Alcohol Drinking Produces Depression-Like Behavior and Reduced Hippocampal Neurogenesis in Mice

Corticotropin-releasing hormone receptors in the medial prefrontal cortex regulate hypothalamic–pituitary–adrenal activity and anxiety-related behavior regardless of prior stress experience

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