Impaired passive avoidance acquisition in Sprague–Dawley and Lewis rats after restraint and cold stress

Klenerová, Věra; Kaminskyi, Oleksii; Šída, Pavel; Krejcí, I; Hliňák, Z; Hynie, S.

doi:10.1016/s0166-4328(02)00093-1

Cited by 25 publications

(24 citation statements)

References 30 publications

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“…However, those more stressful paradigms have been previously shown to change WT animal performance in memory tests such as the Y-maze [11,16]. As expected [17], animals subjected to our confinement stress protocol showed increase serum corticosterone levels, compared to control non-stressed mice (Fig.…”

supporting

confidence: 64%

Short-term memory acquisition in female Huntington's disease mice is vulnerable to acute stress

Renoir

Pang

et al. 2013

Behavioural Brain Research

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Huntington's disease (HD) is a neurodegenerative disorder marked by cognitive, psychiatric and motor decline, and is modifiable by unidentified environmental factors. We examined the effects of stress on cognitive function in R6/1 HD transgenic mice. Utilizing the Y-maze to assess short-term memory, we report that only female HD mice displayed vulnerability to 1h of confinement stress reflected by impaired memory acquisition. This could not be attributed to a different corticosterone response or exploratory behaviour in the task. This is the first demonstration of increased stress susceptibility in an animal model of HD involving a direct negative impact on cognitive function.

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supporting

confidence: 64%

Short-term memory acquisition in female Huntington's disease mice is vulnerable to acute stress

Renoir

Pang

et al. 2013

Behavioural Brain Research

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“…CRH is a critical factor in the response of the brain to stress and has been implicated in mood disorders (Holsboer, 2000). Stresscopin acts primarily at CRH type 2 receptors, and intraperitoneal injection of stresscopin in rats was found to impair memory trace formation and avoidance during a passive avoidance learning task (Klenerova et al, 2003). The upregulation that we observed in depressed brains could represent a homeostatic response to stress and/or other pathology associated with depression.…”

Section: Transduction Of Extracellular Signalsmentioning

confidence: 67%

Gene Expression Profiling in Postmortem Prefrontal Cortex of Major Depressive Disorder

Kang¹,

Adams²,

Simen³

et al. 2007

J. Neurosci.

109

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Investigations of the molecular mechanisms underlying major depressive disorder (MDD) have been hampered by the complexity of brain tissue and sensitivity of gene expression profiling approaches. To address these issues, we used discrete microdissections of postmortem dorsolateral prefrontal cortex (DLPFC) (area 9) and an oligonucleotide (60mer) microarray hybridization procedure that increases sensitivity without RNA amplification. Mixed-effects statistical methods were used to rigorously control for medication usage in the subset of medicated depressed subjects. These analyses yielded a rich profile of dysregulated genes. Two of the most highly dysregulated genes of interest were stresscopin, a neuropeptide involved in stress responses, and Forkhead box D3 (FOXD3), a transcription factor. Secondary cell-based analysis demonstrated that stresscopin and FoxD3 are increased in neurons of DLPFC gray matter of MDD subjects. These findings identify abnormal gene expression in a discrete region of MDD subjects and contribute to further elucidation of the molecular alterations of this complex mood disorder.

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“…With regards to hippocampusdependent tasks, investigators have reported an inverted U-shaped relationship between stress and learning. In human and rodent work, acute stress (or corticosteroid administration) dose-dependently influences declarative (conscious, fact-based) and spatial memory, with short periods of stress (or low doses of corticosteroids) enhancing [31,62,63] and longer periods of stress (or high doses of corticosteroids) impairing [59,[63][64][65][66][67][68] these processes. Studies in humans and rodents have shown that exposure to laboratory stressors (humans: preparation and delivery of a speech, mental arithmetic, cold pressor test; rodents: restraint + tailshock, predator exposure, underwater trauma) of a prolonged duration (typically > 20 min) before or after learning can impair the recall of information.…”

Section: What Is the Shape Of The Dose-response Function Between Strementioning

confidence: 99%

Hormetic and Non-Hormetic Dose-Response Functions in Stress Effects on Memory and Synaptic Plasticity: Issues and Mechanisms

Zoladz¹,

Diamond²

2008

American J. of Pharmacology and Toxicology

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Over a century of behavioral research has shown that stress can exert both positive and negative effects on memory. We have explored the idea that the complex effects of stress on learning and memory can be characterized by hormetic-and non-hormetic dose-response functions, in which stress may either stimulate or impair brain memory mechanisms, depending, in part, on the timing and duration of the stress experience. Extensive work has shown that acute stress or corticosteroid administration has a biphasic effect specifically on hippocampus-dependent learning, memory and synaptic plasticity. We suggest that brief stress exerts a rapid enhancement of memory-related functions of the hippocampus, produced by the amygdala-induced activation of hippocampal synaptic plasticity in conjunction with excitatory effects of neuromodulators, including glucocorticoids, norepinephrine, corticotropin-releasing hormone, acetylcholine and dopamine. We propose that the rapid stress-induced activation of the amygdala-hippocampus brain memory system results in a linear (non-hormetic) dose-response relation between emotional strength and memory formation. In response to more prolonged stress, a delayed inhibition of hippocampal function develops, which can be attributed to compensatory cellular responses which protect hippocampal neurons from excitotoxicity. The inhibition of hippocampal functioning in response to prolonged stress is potentially relevant to the well-described curvilinear (hormetic) dose-response relationship between arousal and memory. In summary, our emphasis on the temporal features of stress-brain interactions addresses how stress can activate, as well as impair, hippocampal functioning to produce differently shaped (nonhormetic/hormetic) stress-memory dose response functions.

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Impaired passive avoidance acquisition in Sprague–Dawley and Lewis rats after restraint and cold stress

Cited by 25 publications

References 30 publications

Short-term memory acquisition in female Huntington's disease mice is vulnerable to acute stress

Short-term memory acquisition in female Huntington's disease mice is vulnerable to acute stress

Gene Expression Profiling in Postmortem Prefrontal Cortex of Major Depressive Disorder

Hormetic and Non-Hormetic Dose-Response Functions in Stress Effects on Memory and Synaptic Plasticity: Issues and Mechanisms

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