Interface of physical and emotional stress regulation through the endogenous opioid system and μ-opioid receptors

Ribeiro, Saulo C. M.; Kennedy, Susan E.; Smith, Yolanda R.; Stohler, Christian S.; Zubieta, Jon Kar

doi:10.1016/j.pnpbp.2005.08.011

Cited by 139 publications

(106 citation statements)

References 234 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Nevertheless, naltrexone strengthened the relationship between negative affect and cold-and shock-induced pain, particularly in the MDD group, consistent with heightened µ-opioid neurotransmission and opioid analgesia in the most distressed cases. These findings support the view that the opioid system, which forms an interface between physical and emotional stress regulation [39], is chronically over-active in the most severe cases of MDD [30]. Further studies are required to determine whether this over-activity promotes opioid tolerance, a factor implicated in the development of chronic pain [9].…”

Section: Discussionsupporting

confidence: 68%

Stress-evoked opioid release inhibits pain in major depressive disorder

Frew

Drummond

2008

Pain

View full text Add to dashboard Cite

To determine whether stress-evoked release of endogenous opioids might account for hypoalgesia in major depressive disorder (MDD), the µ-opioid antagonist naltrexone (50 mg) or placebo was administered double-blind to 24 participants with MDD and to 31 non-depressed controls. Eighty minutes later participants completed a painful foot cold pressor test and, after a 5-minute interval, began a 25-minute arithmetic task interspersed with painful electric shocks. Ten minutes later participants completed a second cold pressor test. Negative affect was greater in participants with MDD than in non-depressed controls throughout the experiment, and increased significantly in both groups during mental arithmetic. Before the math task, naltrexone unmasked direct linear relationships between severity of depression, negative affect while resting quietly, and cold-induced pain in participants with MDD. In contrast, facilitatory effects of naltrexone on cold-and shock-induced pain were greatest in controls with the lowest depression scores. Naltrexone strengthened the relationship between negative affect and shock-induced pain during the math task, particularly in the depressed group, and heightened anxiety in both groups toward the end of the task. Thus, µ-opioid activity apparently masked a positive association between negative affect and pain in the most distressed participants. These findings suggest that psychological distress inhibits pain via stress-evoked release of opioid peptides in severe cases of MDD. In addition, tonic endogenous opioid neurotransmission could inhibit depressive symptoms and pain in people with low depression scores.

show abstract

Section: Discussionsupporting

confidence: 68%

Stress-evoked opioid release inhibits pain in major depressive disorder

Frew

Drummond

2008

Pain

View full text Add to dashboard Cite

show abstract

“…This response may follow a period of active but unsuccessful engagement with a source of stress, and is characterized by quiescence, hypotension, decreased responsiveness to the environment, and prolonged opioid-mediated analgesia (Grau et al, 1981;Keay and Bandler, 2001;Ribeiro et al, 2005). In the present study high levels of discouragement apparently evoked opioid release which, in turn, 'capped' painful sensations during the final cold pressor test.…”

Section: Discussionmentioning

confidence: 56%

“…Uncontrollable aversive events evoke stress-induced analgesia (Amit and Galina, 1986;Fields and Basbaum, 1999) due, in part, to an increase in µ-opioid receptormediated neurotransmission in cortical and subcortical pain control circuits (Ribeiro et al, 2005). Bandura et al (1988) reported that an intense cognitive stressor triggered an opioid-mediated increase in tolerance of cold-induced pain in distressed subjects, whilst this response was absent in subjects who could cope with task demands.…”

Section: Introductionmentioning

confidence: 99%

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

Frew

Drummond

2007

Pain

View full text Add to dashboard Cite

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.

show abstract

“…Thus, in addition to the analgesic, anxiolytic, d-Opioid Receptor Pharmacology and antidepressant actions (Ribeiro et al, 2005;Hsu et al, 2015) that were mentioned in previous sections, opioids also promote cell survival (Hayashi et al, 2002;Ma et al, 2005), cardioprotection (Ikeda et al, 2006;Tsutsumi et al, 2010;Headrick et al, 2015), neuroprotection (He et al, 2013b;Liu et al, 2015), modulation of the immune/inflammatory response (Neptune and Bourne, 1997;Hedin et al, 1999;Sharp, 2006;Wang et al, 2014), and wound healing (Bigliardi-Qi et al, 2006;Iaizzo et al, 2012;Bigliardi et al, 2015). At the cellular level, a majority of these responses are mediated by an evolutionarily conserved set of kinase cascades whose activation has been traditionally associated with receptor tyrosine kinases (RTKs) (Takeda et al, 2011).…”

Section: B D-opioid Receptors and Mitogen-activated Protein Kinase Smentioning

confidence: 99%