Effects of Semax in the Models of Acute Stress

Abstract

Acute stress exposure causes a cascade of neurochemical reactions, leading, in particular, to a change in behavior and increased tolerance to pain in humans and animals. ACTH/MSH-like peptides play an important role in regulating the body’s response to stressful exposures. The aim of the present study was to assess the effects of the ACTH4–10 analogue heptapeptide Semax in various models of acute stress. The effect of intraperitoneal Semax administration at doses of 0.05 and 0.5 mg/kg on changes in behavior and pain sensitivity of Wistar rats in models of inescapable intermittent foot shock stress and forced cold-water swim stress was investigated. To assess the involvement of the endogenous opioid system in the effects of stress, an impact of pretreatment with opioid receptor antagonist naloxone (1 mg/kg) was studied. The stressors used led to an increase in the pain threshold in the paw-pressure test, which indicates the development of stress-induced analgesia (SIA). In addition, rats exposed to stress had an decrease in exploratory behavior and an increase in the anxiety-like behavior in the hole board test. Both Semax and naloxone attenuated SIA in the model of inescapable foot shock stress, but did not affect the value of the pain threshold in the model of forced cold swim stress. Both studied drugs did not affect the behavior of rats in the models of acute stress used. It can be concluded that Semax blocks the opioid form of stress-induced analgesia, but does not affect the behavioral alterations in rats exposed to acute stress.