Contribution of D1- and D2-like dopamine receptors in the ventral tegmental area to the stress-induced analgesia in the animal model of acute pain.

Stressful situations have been observed to enhance pain thresholds, a phenomenon recognized as stress-induced analgesia (SIA). The mechanism underlying SIA involves a combination of endogenous opioids and catecholamines like dopamine. Dopamine in the ventral tegmental area (VTA) is implicated in nociceptive responses. The present study aims to examine the distinct contributions of D1- and D2-like dopamine receptors within the VTA in modulating the impact of exposure to restraint stress (RS) on nociceptive thresholds during the tail-flick test. One hundred five adults male Wistar rats underwent stereotaxic surgery, wherein cannulas were unilaterally implanted into the VTA. Following a recovery period, animals in separate groups received different doses of SCH-23390 or Sulpiride as D1- and D2-like receptor antagonists, respectively, or their corresponding vehicles 5 min before exposure to RS (3 h per rat). Subsequently, a pain threshold assessment was conducted over one hour using a tail-flick apparatus. The obtained findings indicate that exposure to RS, as a form of psychological stress, considerably enhanced antinociceptive behavior in the acute pain model. The reduction of this response was effectively observed through the blockade of dopamine receptors in the VTA, with equal potency attributed to the D2- and D1 like dopamine receptor antagonist. These outcomes provide insights into the potential involvement of the dopaminergic system in pain control under stressful conditions, offering a promising future for developing pharmacological agents and psychological methodologies for pain management.