Hormozi Asef, Zarifkar Asadollah, Rostami Bahar, Naghibalhossaini Fakhraddin
Department of Physiology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Iran J Med Sci. 2019 Sep;44(5):397-405. doi: 10.30476/ijms.2019.44958.
Intense stress can change pain perception and induce hyperalgesia; a phenomenon called stress-induced hyperalgesia (SIH). However, the neurobiological mechanism of this effect remains unclear. The present study aimed to investigate the effect of the spinal cord µ-opioid receptors (MOR) and α2-adrenergic receptors (α2-AR) on pain sensation in rats with SIH.
Eighteen Sprague-Dawley male rats, weighing 200-250 g, were randomly divided into two groups (n=9 per group), namely the control and stress group. The stress group was evoked by random 1-hour daily foot-shock stress (0.8 mA for 10 seconds, 1 minute apart) for 3 weeks using a communication box. The tail-flick and formalin tests were performed in both groups on day 22. The real-time RT-PCR technique was used to observe MOR and α2-AR mRNA levels at the L4-L5 lumbar spinal cord. Statistical analysis was performed using the GraphPad Prism 5 software (San Diego, CA, USA). Student's t test was applied for comparisons between the groups. P<0.05 was considered statistically significant.
There was a significant (P=0.0014) decrease in tail-flick latency in the stress group compared to the control group. Nociceptive behavioral responses to formalin-induced pain in the stress group were significantly increased in the acute (P=0.007) and chronic (P=0.001) phases of the formalin test compared to the control group. A significant reduction was also observed in MOR mRNA level of the stress group compared to the control group (P=0.003). There was no significant difference in α2-AR mRNA level between the stress and control group.
The results indicate that chronic stress can affect nociception and lead to hyperalgesia. The data suggest that decreased expression of spinal cord MOR causes hyperalgesia.
强烈应激可改变痛觉并诱发痛觉过敏；这种现象称为应激诱导的痛觉过敏（SIH）。然而，这种效应的神经生物学机制仍不清楚。本研究旨在探讨脊髓μ-阿片受体（MOR）和α2-肾上腺素能受体（α2-AR）对SIH大鼠痛觉的影响。
将18只体重200 - 250 g的Sprague-Dawley雄性大鼠随机分为两组（每组n = 9），即对照组和应激组。应激组通过使用通讯箱，每天随机进行1小时足部电击应激（0.8 mA，持续10秒，间隔1分钟），持续3周。在第22天对两组进行甩尾和福尔马林试验。采用实时RT-PCR技术观察L4 - L5腰段脊髓中MOR和α2-AR mRNA水平。使用GraphPad Prism 5软件（美国加利福尼亚州圣地亚哥）进行统计分析。采用学生t检验进行组间比较。P < 0.05被认为具有统计学意义。
与对照组相比，应激组的甩尾潜伏期显著缩短（P = 0.0014）。与对照组相比，应激组在福尔马林试验的急性（P = 0.007）和慢性（P = 0.001）期对福尔马林诱导疼痛的伤害性行为反应显著增加。与对照组相比，应激组的MOR mRNA水平也显著降低（P = 0.003）。应激组和对照组之间的α2-AR mRNA水平无显著差异。
结果表明慢性应激可影响痛觉并导致痛觉过敏。数据提示脊髓MOR表达降低导致痛觉过敏。
