Balasubramanian Priya, Subramanian Madhan, Nunez Joseph L, Mohankumar Sheba M J, Mohankumar P S
Neuroendocrine Research Laboratory, Department of Pharmacology & Toxicology, Michigan State University, East Lansing, MI 48824, United States.
Department of Pathobiology & Diagnostic Investigation, Michigan State University, East Lansing, MI 48824, United States.
Behav Brain Res. 2014 Mar 15;261:127-33. doi: 10.1016/j.bbr.2013.12.018. Epub 2013 Dec 19.
Changes in serum estradiol levels are associated with mood disorders in women. However, the underlying mechanisms are not clear. Because alterations in Brain-Derived Neurotrophic Factor (BDNF) and monoamine levels in the hippocampus and amygdala have been associated with anxiety disorders, we hypothesized that chronic treatment with a low dose of estradiol would cause anxiety-like disorder by altering BDNF and monoamine levels in these regions. To test this hypothesis, female rats were sham-implanted (Controls) or implanted with pellets that release estradiol-17β (E2) for 90-days at the rate of 20 ng/day. Animals underwent behavioral tests such as the open field test and elevated plus maze test at the end of treatment. Brains from these animals were frozen, sectioned and the hippocampus, central amygdala and caudate putamen were microdissected and analyzed for monoamine levels using HPLC. BDNF protein levels in these areas were measured using ELISA and BDNF mRNA levels were analyzed using RT-PCR. In the open field test, animals chronically treated with E2 displayed anxiety-like behavior that was marked by a decrease in the number of inner zone crossings and increase in the rate of defecation compared to controls. However, no behavioral changes were observed in the elevated plus maze test. Chronic E2 treatment also decreased BDNF protein and mRNA levels in the central amygdala that was accompanied by a reduction in dopamine levels. No changes were observed in the hippocampus and caudate putamen. These results suggest that BDNF and dopamine in the central amygdala might possibly mediate chronic E2-induced behavioral alterations.
血清雌二醇水平的变化与女性情绪障碍有关。然而,其潜在机制尚不清楚。由于海马体和杏仁核中脑源性神经营养因子(BDNF)和单胺水平的改变与焦虑症有关,我们假设低剂量雌二醇的长期治疗会通过改变这些区域的BDNF和单胺水平而导致焦虑样障碍。为了验证这一假设,对雌性大鼠进行假植入(对照组)或植入以每天20 ng的速率释放17β-雌二醇(E2)的药丸,持续90天。在治疗结束时,对动物进行旷场试验和高架十字迷宫试验等行为测试。将这些动物的大脑冷冻、切片,对海马体、中央杏仁核和尾状壳核进行显微解剖,并使用高效液相色谱法分析单胺水平。使用酶联免疫吸附测定法测量这些区域的BDNF蛋白水平,并使用逆转录聚合酶链反应分析BDNF mRNA水平。在旷场试验中,与对照组相比,长期接受E2治疗的动物表现出焦虑样行为,其特征是内区穿越次数减少和排便率增加。然而,在高架十字迷宫试验中未观察到行为变化。长期E2治疗还降低了中央杏仁核中BDNF蛋白和mRNA水平,同时多巴胺水平降低。在海马体和尾状壳核中未观察到变化。这些结果表明,中央杏仁核中的BDNF和多巴胺可能介导了慢性E2诱导的行为改变。