Excitability of the Nociceptive System in Rats after Blast-Induced Traumatic Brain Injury

Abstract

In a group of healthy adult male albino rats (n=6), we measured pain thresholds under conditions of electrocutaneous stimulation of the limbs (in a chamber with an electrified floor). The animals were subjected to the action of a modeled baroacoustic wave (excess pressure 26–36 kPa) leading to mild blast-induced traumatic brain injury (bTBI). It was found that such a trauma resulted in a long-lasting (up to four weeks) decrease in the above threshold (i.e., in an increase in the sensitivity of the nociceptive system) estimated according to the minimum intensity (μA) of 50-Hz alternating stimulation current evoking a pain-related behavioral response (vocalization). The pain threshold was measured at repeated stimulations of the increasing intensity of animals under light inhalation (halothane) anesthesia. There were reasons to believe that such an effect included two phases, an early (up to three days) and a later more long-lasting phase. The dynamics of the pain threshold in the bTBI group of rats were compared with those in the groups of fully intact rats (intact group) and rats subjected to the procedures of inhalation anesthesia and soft fixation but with no action of the baroacoustic wave (sham group). It is concluded that even mild blast-related trauma leads to significant long-lasting changes in the functioning of the nociceptive and antinociceptive brain neuronal systems, especially in their opioid-mediated components. These shifts develop due to energy deficiency, oxidative stress, and the accompanying mitochondrial damage. Such findings confirm suppositions that blast trauma-related changes in the cerebral opioid systems play a considerable role in the disorders of brain cognitive functions disturbed because of a blast-induced brain injury.