Analgesia and impact induced by anticipation stress: involvement of the endogenous opioid peptide system

Abstract

Anticipation of an unavoidable painful stimulation, i.e. anticipation stress, induces analgesia. This analgesia may result from activation of the endogenous opioid peptide system as it is blocked by naloxone. The present paper characterizes the anticipation stress further by following the kinetics of the analgesia rise, the impact of the stress on the stress-sensitive organs and the involvement of the endogenous opioid peptide system in the anticipation stress effects. Adult male rats exposed repeatedly to placing into a conditioning box followed by a painful stimulation develop analgesia almost immediately after a transfer to the box. Anticipation acts as a specific trigger, no other side stressor is effective. Anticipation stress has a significant impact on stress-sensitive organs: weights of the adrenals increase while those of the thymus and spleen decrease. These changes are associated with a significant increase of plasma corticosterone. Blockade of the endogenous opioid system by naloxone before the exposure to anticipation stress potentiates these stress-induced impacts, especially the decrease of weight of the thymus. Plasma corticosterone levels are not affected by naloxone. During the anticipation stress, the amount of opioid receptors, i.e. of [ 3H]naloxone binding sites, in the hypothalamus, but not in the striatum, decreases. The possible biological role of stress-induced activation of endogenous opioid system, namely the maintenance of the intensity of stress reaction within certain limits and thus the prevention of the self-destructive effects of stress reactions, is discussed.