慢性强迫游泳应激对大鼠情绪和脑细胞外信号调节激酶的影响

为探讨慢性强迫游泳应激对动物情绪和脑组织细胞外信号调节激酶（extracellular signal-regulated kinase, ERK1/2）的影响，动物情绪和脑组织ERK1/2之间的关系，将动物随机分为游泳应激组、装置对照组和控制组。分别对三组大鼠给予相应的干预14天， 然后进行行为观察，免疫印记法测定海马和前脑皮质ERK1/2水平。结果表明强迫游泳应激组和装置对照组都出现明显的情绪障碍。两组大鼠ERK1/2在前脑皮质的表达水平均显著升高，海马无显著变化。前脑皮质ERK2与糖精水摄入量呈显著负相关。提示慢性强迫游泳应激能够诱导大鼠的情绪障碍，提高ERK1/2在前脑皮质的表达水平，ERK1/2与情绪关系密切，可能是脑组织应激性情绪调节的重要生理机制。强迫游泳应激能够导致动物明显的抑郁反应，是比较理想的抑郁动物模型

The Effects of Chronic Forced Swimming Stress on Emotion and Extracellular Signal-regulated Kinase of Brain in Rats

The generic term mitogen-activated protein kinases (MAPKs) is used to denote a family of signal transduction mediators that regulate a diversearrayof cellular functions via activation of a sequential phosphorylation cascade involving a three-protein cassette. Among several MAPKs cascades that have been characterized, the extracellular signal-regulatedkinases 1 and 2 (ERK1/2)are the most widely investigated. ERK1/2are extensively distributed throughout the central nervous system and prominently found in the hippocampus and prefrontal cortex. At present, ERK1/2are being extensively studied in the field of learning and memory. Recent data have demonstrated that ERK has a vital role in the hippocampus-dependent learning and memory and prefrontal cortex-dependent conditioning. It can facilitate learning and memory consolidation and regulate neuronal plasticity. However, there is rather little evidence concerning the role of ERK1/2in stress response and emotional regulation. The purpose of the present study was to detect the effects of chronic forced swimming stress on emotion and ERK1/2 in the hippocampus and the prefrontal cortex in rats and to determine the relation between emotion and ERK1/2 of brain. Thirty rats were randomly divided into three groups. They were the swimming stress group, apparatus control group,and the control group. The stressed animals received swimming stress for 5 minutes once a day for 14 days. The apparatus controls were placed in a novel environment for 5 minutes once a day for 14 consecutive days. The controls were free of stress. After stress, rats were tested with an open-field, elevated-plus maze and saccharin preferencetest. They were then decapitated and dissected to detect the ERK1/2 of the hippocampus and prefrontal cortex with blotting. It was found that both the swimming stress group and the apparatus control group showed significant emotional disorders. The body weight gain of the stressed group was significantly lower than that of the controlgroup and the apparatus controls. The defecation of the apparatus controls was more than that of the controlgroup and the stressed group. The locomotion of the stressed group was significantly lower than that of the other two groups. Compared to the controls, the stressed animals spent a shortertime in open arms and longer time in closed arms. Thesaccharine solution consumed and the ratio of the saccharine solution consumed to the total liquid consumed of both the stressed group and the apparatus controls were significantly lower than that of the controlgroup. There were enhanced levels of ERK1/2 in the prefrontal cortex of the stressed group and the apparatus controls, with no change in the hippocampus. The ERK2 level of the prefrontal cortex was negatively correlated withthe amount of the saccharin solution consumed. The results suggested chronic swimming stress could induce emotional disorders and increase the level of ERK1/2 in the prefrontal cortex. ERK1/2 was closely linked toemotional responseand could provide new insight into the mechanism underlying protective reaction under stressful situations.