Role of endogenous opioid system in the regulation of the stress response

Drolet, Guy; Dumont, Éric; Gosselin, Isabelle; Kinkead, Richard; Laforest, Sylvie; Trottier, Jean-François

doi:10.1016/s0278-5846(01)00161-0

Cited by 368 publications

(246 citation statements)

References 71 publications

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“…Thus, activation of the endogenous opioid system during psychological stress could suppress the affective and sensory components of pain independently. The presence of opioid peptides and receptor sites in areas of the brain that modulate responses to psychological stress is consistent with this idea (Drolet et al, 2001). …”

Section: Introductionsupporting

confidence: 62%

Negative affect, pain and sex: The role of endogenous opioids

Frew

Drummond

2007

Pain

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Opioid neurotransmission modulates pain and negative affect during psychological stress.To determine whether these effects differ between men and women, the opioid receptor antagonist naltrexone or placebo was administered double-blind to 21 men and 22 women before they completed 30 minutes of difficult mental arithmetic. To heighten negative affect, participants received seven moderately noxious electric shocks during the math task, which were believed to be contingent upon performance. Before and after the math task, participants rated pain intensity and unpleasantness while their left hand was immersed in 2 o C water for up to 4 minutes. Anxiety, discouragement and anger were also rated before, during and after the math task. Tolerance of cold-induced pain was greater in men, whereas discouragement during the math task was greater in women. Opioid blockade did not influence ratings of negative affect, which increased in line with the intensity and unpleasantness of shock-induced pain. The intensity and unpleasantness of cold-induced pain increased after the math task only in women administered naltrexone.Within the naltrexone condition, pain ratings increased most in the most discouraged subjects. However, this relationship was absent in placebo recipients, implying that the hyperalgesic effect of psychological distress was tempered by opioid release. Greater stress-evoked discouragement in women than men may explain why cold-induced pain increased after the math task only in women administered naltrexone.

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Section: Introductionsupporting

confidence: 62%

Negative affect, pain and sex: The role of endogenous opioids

Frew

Drummond

2007

Pain

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“…The mechanisms involved in this process still remained controversial. Numerous studies support the idea that the endogenous opioid peptide system contributes to the mediation, modulation, and regulation of stress responses by either: 1) activation of the endocrine (HPA axis), 2) modulation of the autonomic nervous system, or 3) a direct effect on immune cells (13,21,22). The families of endogenous opioids identified to date are the endorphins, the enkephalins, and the dynorphins.…”

Section: Discussionmentioning

confidence: 98%

μ-Opioid Receptor Mediates Chronic Restraint Stress-Induced Lymphocyte Apoptosis

Wang

Charboneau

Barke

et al. 2002

The Journal of Immunology

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Psychological stress is associated with immunosuppression in both humans and animals. Although it was well established that psychological stressors stimulate the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, resulting in the release of various hormones and neurotransmitters, the mechanisms underlying these phenomena are poorly understood. In this study, μ-opioid receptor knockout (MORKO) mice were used to investigate whether the μ-opioid receptor mediates the immunosuppression induced by restraint stress. Our results showed that wild-type (WT) mice subjected to chronic 12-h daily restraint stress for 2 days exhibited a significant decrease in splenocyte number with a substantial increase in apoptosis and CD95 (Fas/APO-1) expression of splenocytes. The effects are essentially abolished in MORKO mice. Furthermore, inhibition of splenic lymphocyte proliferation, IL-2, and IFN-γ production induced by restraint stress in WT mice was also significantly abolished in MORKO mice. Interestingly, both stressed WT and MORKO mice showed a significant elevation in plasma corticosterone and pituitary proopiomelanocortin mRNA expression, although the increase was significantly lower in MORKO mice. Adrenalectomy did not reverse restraint stress-induced immunosuppression in WT mice. These data clearly established that the μ-opioid receptor is involved in restraint stress-induced immune alterations via a mechanism of apoptotic cell death, and that the effect is not mediated exclusively through the glucocorticoid pathway.

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“…Enkephalins belong to the family of endogenous opioids and are involved in, e.g., reward/ motivation (Barbano and Cador 2007) and the regulation of the stress response (Drolet et al 2001). An involvement of the endogenous opioidergic system in the mediation of several symptoms of depression has long been discussed, and it has been shown that enkephalin catabolism inhibitors (RB101) induce antidepressant-like effects (Roques 2000).…”

Section: Paroxetine Enhances Preproenkephalin 1 (Penk1) Expressionmentioning

confidence: 99%

Profiling of behavioral changes and hippocampal gene expression in mice chronically treated with the SSRI paroxetine

et al. 2008

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Introduction Monoamine-based antidepressants inhibit neurotransmitter reuptake within short time. However, it commonly takes several weeks until clinical symptoms start to resolve-indicating the involvement of effects distant from reuptake inhibition. Objective To unravel other mechanisms involved in drug action, a "reverse" pharmacological approach was applied to determine antidepressant-induced alterations of hippocampal gene expression. Materials and methodsThe behavioral response to longterm paroxetine administration of male DBA/2Ola mice was assessed by the forced swim test (FST), the modified hole board (mHB), and the dark/light box. Hippocampi of test-naive mice were dissected, and changes in gene expression by paroxetine treatment were investigated by means of microarray technology. Results and discussion Robust effects of paroxetine on passive stress-coping behavior in the FST were observed. Furthermore, anxiolytic properties of long-term antidepressant treatment could be identified in DBA mice in both, the mHB and dark/light box. Analysis of microarray results revealed a list of 60 genes differentially regulated by chronic paroxetine treatment. Preproenkephalin 1 and inhibin beta-A showed the highest level of transcriptional change. Furthermore, a number of candidates involved in neuroplasticity/neurogenesis emerged (e.g., Bdnf, Gfap, Vim, Sox11, Egr1, Stat3). Seven selected candidates were confirmed by in situ hybridization. Additional immunofluorescence colocalization studies of GFAP and vimentin showed more positive cells to be detected in long-term paroxetine-treated DBA mice. Conclusion Candidate genes identified in the current study using a mouse strain validated for its responsiveness to long-term paroxetine treatment add, in our opinion, to unraveling the mechanism of action of paroxetine as a representative for SSRIs.

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Role of endogenous opioid system in the regulation of the stress response

Cited by 368 publications

References 71 publications

Negative affect, pain and sex: The role of endogenous opioids

Negative affect, pain and sex: The role of endogenous opioids

μ-Opioid Receptor Mediates Chronic Restraint Stress-Induced Lymphocyte Apoptosis

Profiling of behavioral changes and hippocampal gene expression in mice chronically treated with the SSRI paroxetine

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