DHEA administration modulates stress-induced analgesia in rats

DHEA administration modulates stress-induced analgesia in rats
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DOI:
10.1016/j.physbeh.2016.02.004
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发表时间:
2016-04-01
影响因子:
2.9
通讯作者:
Marques Ribeiro, Maria Flavia
Marques Ribeiro, Maria Flavia
中科院分区:
医学3区
文献类型:
--
作者:
Cecconello, Ana Lucia;Torres, Iraci L. S.;Marques Ribeiro, Maria Flavia

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适应性应激反应的一个重要方面是在应激暴露期间或之后发生的疼痛反应抑制,这通常被称为急性应激性镇痛。脱氢表雄酮 (DHEA) 参与调节适应性应激反应,改变 HPA 轴活动。 DHEA 对 HPA 轴活性的影响取决于状态,并使用参与调节急性应激诱导镇痛的相同系统。研究了 DHEA 对伤害感受的影响;然而,DHEA 对应激性镇痛的影响尚不清楚。因此,本研究的目的是评估 DHEA 对应激性镇痛的作用,并确定与应激源刺激相关的激素给药最佳时间。对动物进行单次暴露约束1小时的应激,并通过应激前单次注射或应激后单次注射接受DHEA治疗。用甩尾装置评估伤害感受。测量血清皮质酮水平。在暴露于压力之前给予 DHEA 可延长急性压力引起的镇痛效果。当应激后给予 DHEA 时,没有观察到这种效应。对非应激大鼠进行 DHEA 治疗不会改变伤害感受阈值,表明 DHEA 对伤害感受的影响是状态依赖性的。注射 DHEA 与暴露于急性应激具有相同的效果,都会增加皮质酮水平。总之,DHEA 的急性治疗模拟了以 HPA 轴活性增加为指标的急性应激反应。在应激暴露前使用 DHEA 治疗可能会促进适应性应激反应,延长急性应激诱导的镇痛时间,这可能是临床感兴趣的治疗策略。 (C) 2016 Elsevier Inc. 保留所有权利。
An important aspect of adaptive stress response is the pain response suppression that occurs during or following stress exposure, which is often referred to as acute stress-induced analgesia. Dehydroepiandrosterone (DHEA) participates in the modulation of adaptive stress response, changing the HPA axis activity. The effect of DHEA on the HPA axis activity is dependent on the state and uses the same systems that participate in the regulation of acute stress-induced analgesia. The impact of DHEA on nociception has been studied; however, the effect of DHEA on stress-induced analgesia is not known. Thus, the aim of the present study was to evaluate the effect of DHEA on stress-induced analgesia and determine the best time for hormone administration in relation to exposure to stressor stimulus. The animals were stressed by restraint for 1 h in a single exposure and received treatment with DHEA by a single injection before the stress or a single injection after the stress. Nociception was assessed with a tail-flick apparatus. Serum corticosterone levels were measured. DHEA administered before exposure to stress prolonged the acute stress-induced analgesia. This effect was not observed when the DHEA was administered after the stress. DHEA treatment in non-stressed rats did not alter the nociceptive threshold, suggesting that the DHEA effect on nociception is state-dependent. The injection of DHEA had the same effect as exposure to acute stress, with both increasing the levels of corticosterone. In conclusion, acute treatment with DHEA mimics the response to acute stress indexed by an increase in activity of the HPA axis. The treatment with DHEA before stress exposure may facilitate adaptive stress response, prolonging acute stress-induced analgesia, which may be a therapeutic strategy of interest to clinics. (C) 2016 Elsevier Inc. All rights reserved.