Activation of .MU.-Opioid Pathway Is Associated with the Canceling Effect of Footshock Stimulus on the Restraint Stress-Induced Inhibition of Small Intestinal Motility in Rats.

Abstract

We previously reported that small intestinal motility was significantly inhibited by restraint stress, but not by footshock stress. In the present study, we found that plasma b b-endorphin levels were more significantly elevated by footshock stress than restraint stress, and that preloading of footshock stimulus canceled the inhibition of small intestinal motility by restraint stress. Pretreatment with the m m-opioid receptor antagonist naltrexone significantly attenuated this canceling effect of footshock stimulus. These results suggest that footshock stimulus may cancel the inhibition of small intestinal motility by restraint stress via activation of m m-opioid receptors.

Mechanism of Inhibition of Small Intestinal Motility by Restraint Stress Differs from That with Norepinephrine Treatment in Rats.

“…It is suggested that the restraint stress-induced inhibition of small intestinal motility does not occur only by stimulation of the sympathetic nervous system, since inhibition of the opioidergic pathway may be also involved. 22) With restraint stress, it is possible that a 2 -adrenergic action is inhibited, or alternatively that b 3 -adrenergic action predominates as a result of neural interactions between nervous systems activated by the stress. …”

The influence of stress and methionine-enkephalin on macrophage functions in two inbred rat strains

“…Of relevance to our current study are the findings of Tsukada et al (2001) who showed that footshock stress induced a significantly greater increase in the levels of endogenous opioid peptides (up to 800 fM in plasma) than a milder form of psychological stress (up to 300 fM). In addition, it has been shown that stress involving mediators corticotropin-releasing hormone and catecholamines (Cabot et al, 2001;Mousa et al, 2004) enhances the release of biologically active pro-enkephalinderived peptides from macrophages which can then act in an autocrine/paracrine manner (Saravia et al, 1998).…”

The Effects of Corticosterone and Beta-Endorphin on Adherence, Phagocytosis and Hydrogen Peroxide Production of Macrophages Isolated from Dark Agouti Rats Exposed to Acute Stress

“…Since ES is delivered as a group of unpredictable, inescapable and uncontrollable signals hindering the rat's ability to cope with the stressor, it is also considered a psychological stressor. Taken together, ES exposure results in motivational and learning deficits, a reduction in social dominance [31][32][33] , increases in corticosterone and ␤ -endorphin levels [22,25] and profound immunological changes [30,34,35] .…”

“…The objective of the present study was to investigate the effect of acute stressful events known to induce the secretion of corticosterone [22,23] and opioid peptides [24,25] on adherence, phagocytosis and production of hydrogen peroxide of macrophages obtained from rats of the DA strain. We have also studied the in vitro effects of corticosterone and the opioid peptide ␤ -endorphin on macrophage function in order to mimic the influence of stress at cellular level.…”