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Inescapable Stress (inescapable + stress)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Chronic Pain, Chronic Stress and Depression: Coincidence or Consequence?

JOURNAL OF NEUROENDOCRINOLOGY, Issue 12 2001
G. Blackburn-Munro
Abstract Chronic pain and depressive illness are debilitating disease states that are variably resistant to currently available therapeutic agents. Animal models of chronic pain are associated with activation of the hypothalamo-pituitary-adrenal (HPA) axis, upon which chronic pain acts as an inescapable stressor. Inescapable stress is also associated with ,depressive-like' symptoms in experimental animals. Based on reports of the comorbidity between chronic pain and depressive illness in human patients, it is possible that these disease states are linked, via chronic stress-induced HPA dysfunction. Here, we discuss the possible involvement of the HPA axis in the aetiology of both chronic pain and clinical depression, and suggest a strategy for the development of novel pharmacotherapies. [source]

Stress reverses plasticity in the pathway projecting from the ventromedial prefrontal cortex to the basolateral amygdala

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2006
Mouna Maroun
Abstract We have previously shown that high-frequency stimulation to the basolateral amygdala (BLA) induces long-term potentiation (LTP) in the ventromedial prefrontal cortex (vmPFC) and that prior exposure to inescapable stress inhibits the induction of LTP in this pathway [Maroun & Richter-Levin (2003)J. Neurosci., 23, 4406,4409]. Here, we show that the reciprocal pathway projecting from the vmPFC to the BLA is resistant to the induction of LTP. Conversely, long-term depression (LTD) is robustly induced in the BLA in response to low-frequency stimulation to the vmPFC. Furthermore, prior exposure to inescapable stress reverses plasticity in this pathway, resulting in the promotion of LTP and the inhibition of LTD. Our findings suggest that, under normal and safe conditions, the vmPFC is unable to exert excitatory synaptic plasticity over the BLA; rather, LTD, which encodes memory of safety in the BLA, is favoured. Following stressful experiences, LTP in the BLA is promoted to encode memory of fear. [source]

,-Endorphin Mediates Behavioral Despair and the Effect of Ethanol on the Tail Suspension Test in Mice

ALCOHOLISM, Issue 6 2010
Elizabeth T. Barfield
Background:, The opioid peptide ,-endorphin (,-E) is synthesized and released in response to stressful stimuli as well as acute alcohol administration. The release of ,-E following exposure to an inescapable aversive situation may mediate behaviors that contribute to allostasis of the stress response. The present study examines the effects of ,-E on immobility in assays involving inescapable stress, both under basal conditions and after acute administration of EtOH. Methods:, Female and male transgenic mice with varying capacities to translate ,-E were subjected to either the forced swim (FST, Experiment 1) or the tail suspension test (TST, Experiment 2). In Experiment 3, mice were divided into three groups based on hormonal status (male, female-estrous, and female-nonestrous) and injected with either 1 g/kg EtOH or equivolume saline 14 minutes prior to behavioral assessment on the TST. Results:, Experiments 1 and 2 demonstrated a direct relationship between ,-E levels and immobility. There were also sex differences in behavior in these tests, with males displaying more immobility than females. A main effect of genotype in Experiment 3 replicated findings in Experiments 1 and 2. There was also an effect of EtOH (increasing immobility) and a significant interaction reflecting a particularly robust effect of the drug in mice with low ,-E. In addition, there were interactions between ,-E, EtOH effects, and hormonal status. Conclusions:, These findings support the contention that ,-E moderates behavioral responses to stressful stimuli and suggest a role for this peptide in coping behavior. Furthermore, the effects of EtOH on the response to stress may be mediated by ,-E. Sex differences in this influence may contribute to sex differences in disease susceptibility and expression. [source]

5-HT1A receptors are involved in the cannabidiol-induced attenuation of behavioural and cardiovascular responses to acute restraint stress in rats

BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2009
Leonardo B.M. Resstel
Background and purpose:, Cannabidiol (CBD) is a non-psychotomimetic compound from Cannabis sativa which induces anxiolytic- and antipsychotic-like effects in rodents. These effects could be mediated by facilitation of the endocannabinoid system or by the activation of 5-HT1A receptors. As either of these mechanisms could promote adaptation to inescapable stress, the aim of the present work was to test the hypothesis that CBD would attenuate the autonomic and behavioural consequences of restraint stress (RS). We also investigated if the responses to CBD depended on activation of 5-HT1A receptors. Experimental approach:, Male Wistar rats received i.p. injections of vehicle or CBD (1, 10 or 20 mg kg,1) and 30 min later were submitted to 60 min of restraint where their cardiovascular responses were recorded. The protocol of the second experiment was similar to the first one except that animals received i.p. injections of the 5-HT1A receptor antagonist WAY100635 (0.1 mg kg,1) before CBD treatment and exposure to restraint. 24 h later they were also tested in the elevated plus-maze (EPM), an animal model of anxiety. Key results:, Exposure to RS increased blood pressure and heart rate and induced an anxiogenic response in the EPM 24 h later. These effects were attenuated by CBD. WAY100635 by itself did not change the cardiovascular and anxiogenic response to RS, but blocked the effects of CBD. Conclusion and implications:, The results suggest that CBD can attenuate acute autonomic responses to stress and its delayed emotional consequences by facilitating 5-HT1A receptor-mediated neurotransmission. [source]