Jochum Thomas, Boettger Michael Karl, Wigger Alexandra, Beiderbeck Daniela, Neumann Inga D, Landgraf Rainer, Sauer Heinrich, Bär Karl-Jürgen
Department of Psychiatry and Psychotherapy, Friedrich-Schiller-University Jena, Philosophenweg 3, 07743 Jena, Federal Republic of Germany.
Behav Brain Res. 2007 Oct 1;183(1):18-24. doi: 10.1016/j.bbr.2007.05.022. Epub 2007 May 24.
Complex interactions between pain perception, anxiety and depressive symptoms have repeatedly been described. However, pathophysiological or biochemical mechanisms underlying the alterations of pain perception in patients suffering from anxiety or depression still remain a matter of debate. Thus, we aimed to perform an investigation on pain perception in an animal model of extremes in anxiety-related behaviour, which might provide a tool for future studies. Here, thermal pain thresholds were obtained from rats with a genetic predisposition to high anxiety-related behaviour (HAB), including signs of comorbid depression-like behaviour and from controls (low-anxiety rats (LAB); cross-bred HAB and LAB rats; Wistar rats). Furthermore, the effect of eight-week antidepressive treatment using citalopram and of short-term anxiolytic treatment with diazepam on pain-related behaviour was assessed. Simultaneously, anxiety-related behaviour was monitored. At baseline, HAB animals showed 35% higher thresholds for thermal pain than controls. These were normalized to control levels after eight weeks of continuous citalopram treatment paralleled by a reduction of anxiety-related behaviour, but also acutely after diazepam administration. Overall, thermal pain thresholds in HAB animals are shifted in a similar fashion as seen in patients suffering from major depressive disorder. Antidepressive, as well as anxiolytic treatments, attenuated these differences. As the relative importance of the factors anxiety and depression cannot be derived from this study with certainty, extending these investigations to additional animal models might represent a valuable tool for future investigations concerning the interrelations between anxiety, depression, and pain at a molecular level.
疼痛感知、焦虑和抑郁症状之间的复杂相互作用已被多次描述。然而，焦虑或抑郁患者疼痛感知改变背后的病理生理或生化机制仍存在争议。因此，我们旨在对具有极端焦虑相关行为的动物模型的疼痛感知进行研究，这可能为未来的研究提供一种工具。在这里，我们从具有高焦虑相关行为遗传倾向（HAB）的大鼠（包括共病抑郁样行为的迹象）以及对照组（低焦虑大鼠（LAB）；杂交HAB和LAB大鼠；Wistar大鼠）中获得热痛阈值。此外，评估了使用西酞普兰进行八周抗抑郁治疗以及使用地西泮进行短期抗焦虑治疗对疼痛相关行为的影响。同时，监测焦虑相关行为。在基线时，HAB动物的热痛阈值比对照组高35%。在连续八周的西酞普兰治疗后，这些阈值恢复到对照水平，同时焦虑相关行为减少，在地西泮给药后也急性恢复到对照水平。总体而言，HAB动物的热痛阈值变化方式与重度抑郁症患者相似。抗抑郁治疗和抗焦虑治疗都减弱了这些差异。由于本研究无法确定焦虑和抑郁因素的相对重要性，将这些研究扩展到其他动物模型可能是未来在分子水平上研究焦虑、抑郁和疼痛之间相互关系的有价值工具。
