Department of Neuroscience, School of Medicine, Ewha Womans University, Yangchon-ku, Seoul, Korea.
Neurochem Res. 2011 Feb;36(2):258-67. doi: 10.1007/s11064-010-0313-1. Epub 2010 Nov 13.
Stress causes endocrinological changes and leads to induce anxiety. It was determined the anxiety and stress-related endocrinological changes through the observation of the level of glucocorticoid and sphingolipid metabolites in serum after stress. Immobilized stress and electric shock was applied to rats for 7 days. This study investigated the induction of anxiety, changes of TH and pERK expression in cortex and amygdala after stress. Also it was determined the changes of glucocorticoid and anxiety when the rats were given stress after amygdala lesion. The stress-given rats spent a lesser percentage of time significantly in the open arm than the control rats. The elevated level of glucocorticoid after stress was suppressed in amygdala lesion group. The expression of TH in the amygdala was decreased, but the expression of TH was not changed in the cortex after stress. To investigate the changes in sphingolipid metabolites after stress, the levels of sphingosine and the phosphate form of sphingolipid (So-1-P) were analyzed in serum. The level of So-1-P was elevated after stress and anxiety was observed after the So-1-P infusion (100 pmol/10 μl/h, i.c.v., for 7 days). Continuous infusion of So-1-P for 7 days led to the significant decrease of TH expression in the amygdala. In conclusion, the results of this study indicate that the lesion of amygdala suppressed the stress-induced anxiety and elevation of glucocorticoid in serum. It was also observed that expression of TH in amygdala as well as increased levels of glucocorticoid in serum might be responsible biomarker, at least in part, of chronic stress. These results suggest that the elevation of So-1-P might be involved in induction of anxiety during stress by the modulation of dopaminergic system in amygdala.
应激导致内分泌变化，并引发焦虑。通过观察应激后血清中糖皮质激素和神经鞘脂代谢物的水平来确定与焦虑相关的内分泌变化。将束缚应激和电击应用于大鼠 7 天。本研究探讨了应激后焦虑的诱导、皮质和杏仁核中 TH 和 pERK 表达的变化，以及在杏仁核损伤后给予大鼠应激时糖皮质激素和焦虑的变化。给予应激的大鼠在开放臂上花费的时间明显少于对照组大鼠。杏仁核损伤组应激后糖皮质激素水平升高受到抑制。应激后杏仁核中 TH 的表达减少，但皮质中 TH 的表达没有变化。为了研究应激后神经鞘脂代谢物的变化，分析了血清中神经鞘氨醇和神经鞘脂磷酸酯（So-1-P）的水平。应激后 So-1-P 水平升高，观察到 So-1-P 输注（100 pmol/10 μl/h，侧脑室，持续 7 天）后出现焦虑。连续 7 天输注 So-1-P 导致杏仁核中 TH 表达显著下降。总之，本研究结果表明，杏仁核损伤抑制了应激引起的焦虑和血清中糖皮质激素的升高。还观察到，杏仁核中 TH 的表达以及血清中糖皮质激素水平的升高可能是慢性应激的至少部分生物标志物。这些结果表明，So-1-P 的升高可能通过调节杏仁核中的多巴胺能系统参与应激时的焦虑诱导。
