睡眠剥夺抗抑郁机制中腺苷及其受体对海马蛋白激酶A的影响

目的：研究快眼动睡眠剥夺（麟D）抗抑郁机制中腺苷及其受体对海马蛋白激酶（PK）A的影响。方法：成年雄性SD大鼠分为正常对照组（8只）和应激模型组（48只。经21d慢性不可预见性应激（CUS）、蔗糖水消耗和强迫游泳实验测试后再随机分为抑郁模型组、睡眠剥夺组、水环境对照组、Ns对照组、腺苷A1受体拮抗剂组、腺苷A2A受体拈抗剂组（每组8只），行72hREMSD，以免疫组化的方法检测海马PKA的表达）。结果：应激模型组蔗糖水消耗量明显降低（P〈0．01），强迫游泳实验中的不动时间明显增加（P〈0．01）。海马CAI区PKA的表达无统计学意义，抑郁模型组海马CA3区PKA水平明显降低（P〈0．01）。与抑郁模型组比，睡眠剥夺组、腺苷A1受体拮抗剂组海马CA3区PKA水平升高（P〈0．01，P〈0．05），腺苷A2A受体拮抗剂组无统计学意义。结论：72hREMSD可以提高抑郁模型海马CA3区PKA的表达，在72hREMSD过程中腺苷A1受体的失活可使海马CA3区PKA的表达增加，而腺苷A2A受体失活则无此效应。

Effects on Protein Kinase A in Hippocampus by Adenosine and Its Receptors in Antidepressive Mechanism of Sleep Deprivation

Objective： To investigate the effects of protein kinase（PK）A in hippocampus by adenosine and its receptors in antidepressive mechanism of rapid-eye-movement sleep deprivation（REMSD）. Methods： The adult males SD rats were divided into normal control group（n =8）and stress-model group（ n =48）, which was subdivided into depression model group, sleep deprivation group, water surrounding control group, NS control group, adenosine A1, A2A receptor antagonist groups, 8 for each group, by chronic unpredicted stress, sucrose consumption and forced swimming test at 21 days. After 72 hours REMSD, the level of PKA in hippocampus was detected by immunohistochemistry. Results： In the CUS group, the sucrose consumption was lower than that in the control group（P 〈 0.01）, and the immobility time was longer than that in the control group（ P 〈 0.01）. There was no statistical significance for PKA in hippocampus CA1 among groups, and the level of PKA in hippocampus CA3 in the depression model group was decreased（ P 〈 0.01）. Compared with depression model group, the level of PKA in hippocampus CA3 in the adenosine A2A receptor antagonist and sleep deprivation groups was significantly increased（ P 〈 0.01, P 〈 0.05）. There was no statistical significance in the adenosine A2A receptor antagonist group. Conclusion： The level of PKA in hippocampus CA3 is increased by the 72 hours REMSD. When the adenosine A1 receptor is inactivated, 72 hours REMSD can lead to the increase of PKA in hippocampus CA3, but any changes can be observed when the adenosine A2A receptor is inactivated.