Jiang Zhao-Cai, Qi Wei-Jing, Wang Jin-Yan, Luo Fei
Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing 100101, China ; University of Chinese Academy of Sciences, Beijing 100039, China.
Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing 100101, China ; Department of Psychology, Guang'anmen Hospital, Chinese Academy of Chinese Medical Sciences, Beijing 100035, China.
ScientificWorldJournal. 2014 Jan 23;2014:405736. doi: 10.1155/2014/405736. eCollection 2014.
Previous studies have shown that depressed patients as well as animal models of depression exhibit decreased sensitivity to evoked pain stimuli, and serotonin is indicated to be involved in depression-induced hypoalgesia. The purpose of this study was to investigate the potential role of 5-HT1A receptor in the depression-induced hypoalgesia. Acute or chronic administration of 5-HT1A receptor agonist, 8-OH-DPAT, was performed in olfactory bulbectomy (OB) and sham-operated rats. The depression-like behavior and pain thresholds were measured using open-field test and radiant heat thermal pain test, respectively. We found that acute administration of 8-OH-DPAT increased locomotor activity and pain thresholds in the sham rats but had no effect on the OB rats. In contrast, chronic administration of 8-OH-DPAT reduced locomotor activity and pain thresholds and restored them to normal level. Increased pain thresholds were also observed in the sham rats after the chronic administration. These results demonstrated that chronic administration of 8-OH-DPAT reversed the depression-induced decrease in pain sensitivity in rats, suggesting that 5-HT1A receptor may play a role in the depression-associated hypoalgesia.
先前的研究表明,抑郁症患者以及抑郁症动物模型对诱发的疼痛刺激的敏感性降低,并且血清素被认为与抑郁症诱导的痛觉减退有关。本研究的目的是调查5-HT1A受体在抑郁症诱导的痛觉减退中的潜在作用。在嗅球切除术(OB)大鼠和假手术大鼠中急性或慢性给予5-HT1A受体激动剂8-OH-DPAT。分别使用旷场试验和辐射热热痛试验测量抑郁样行为和疼痛阈值。我们发现,急性给予8-OH-DPAT可增加假手术大鼠的运动活性和疼痛阈值,但对OB大鼠没有影响。相反,慢性给予8-OH-DPAT可降低运动活性和疼痛阈值,并将它们恢复到正常水平。慢性给药后,假手术大鼠的疼痛阈值也升高。这些结果表明,慢性给予8-OH-DPAT可逆转抑郁症诱导的大鼠疼痛敏感性降低,表明5-HT1A受体可能在抑郁症相关的痛觉减退中起作用。