Marini Francesca, Pozzato Chiara, Andreetta Valentino, Jansson Birger, Arban Roberto, Domenici Enrico, Carboni Lucia
Department of Medicine and Public Health, Section of Pharmacology, University of Verona, Verona, Italy.
Brain Res. 2006 Jan 5;1067(1):25-35. doi: 10.1016/j.brainres.2005.10.002. Epub 2005 Dec 15.
Stressful life events are able to induce long-term modifications in physiological and neuroendocrine parameters that are related to the onset of several psychiatric disorders. To gain information on molecular modifications involved in long-term changes triggered by stress, we evaluated gene expression in the hippocampus of rats exposed to a single social defeat session. In the social defeat model, the experimental animal is defeated by a dominant male. The defeat induced an increase in body temperature, in distress vocalisations, in serum corticosterone levels and in anxiety-related behaviour measured with an open field test applied 6 h after the exposure to the dominant rat. In the open field test, anxiety-related behaviours were not detectable anymore 30 h after the exposure to the dominant rat and mRNA levels were evaluated at this time-point. The mRNA levels of genes modulated by stress (corticotropin-releasing factor; corticotropin-releasing factor receptor 1; corticotropin-releasing factor binding protein; mineralocorticoid and glucocorticoid receptors; Ca2+/calmodulin-dependent protein kinase-like kinase; Krox20; Bcl-2) and control genes (glyceraldehyde-3-phosphate dehydrogenase; beta-actin and cyclophilin A) were measured with real-time reverse transcription polymerase chain reaction. Corticotropin-releasing factor and glucocorticoid receptor mRNA levels were significantly modulated by the stress procedure, both genes showing an increase in rats exposed to a social defeat. No expression level differences were detected for the other genes. In conclusion, we report that 30 h after an acute social stress, a modification in mRNA levels can be detected in rat hippocampus, thus suggesting potential candidate genes involved in mediating long-term responses.
应激性生活事件能够引起生理和神经内分泌参数的长期改变，这些改变与多种精神障碍的发病有关。为了获取有关应激引发的长期变化所涉及的分子改变的信息，我们评估了经历单次社会挫败的大鼠海马体中的基因表达。在社会挫败模型中，实验动物被一只占主导地位的雄性大鼠击败。这种挫败导致体温升高、痛苦叫声增加、血清皮质酮水平升高以及在接触占主导地位的大鼠6小时后通过旷场试验测量的焦虑相关行为增加。在旷场试验中，接触占主导地位的大鼠30小时后不再能检测到焦虑相关行为，此时评估mRNA水平。通过实时逆转录聚合酶链反应测量应激调节基因（促肾上腺皮质激素释放因子；促肾上腺皮质激素释放因子受体1；促肾上腺皮质激素释放因子结合蛋白；盐皮质激素和糖皮质激素受体；Ca2+/钙调蛋白依赖性蛋白激酶样激酶；Krox20；Bcl-2）和对照基因（甘油醛-3-磷酸脱氢酶；β-肌动蛋白和亲环蛋白A）的mRNA水平。应激过程显著调节了促肾上腺皮质激素释放因子和糖皮质激素受体的mRNA水平，这两个基因在经历社会挫败的大鼠中均表现出增加。其他基因未检测到表达水平差异。总之，我们报告在急性社会应激30小时后，大鼠海马体中可检测到mRNA水平的改变，从而提示了参与介导长期反应的潜在候选基因。
