Von Frijtag J C, Kamal A, Reijmers L G, Schrama L H, van den Bos R, Spruijt B M
Department of Animals & Society, Utrecht University, Yalelaan 17, 3584 CL, Utrecht, The Netherlands.
Neurosci Lett. 2001 Aug 31;309(3):153-6. doi: 10.1016/s0304-3940(01)02062-6.
In the present study, we investigated whether synaptic plasticity changes in the hippocampus of depressive-like socially stressed rats could be reversed by chronic antidepressant treatment. To that end, rats were either defeated and subsequently individually housed or subjected to control treatment followed by social housing. After a period of at least 3 months, rats were either treated chronically with imipramine (20 mg/kg per day, per os for at least 3 months) or the solvent solution (i.e. water). Then, long-term potentiation and depression were measured in the CA1 region of the hippocampus in vitro. Chronic imipramine treatment partially restored the attenuated induction of long-term potentiation and suppressed the facilitation of long-term depression-induction in socially stressed rats. The altered synaptic plasticity after social stress is discussed in relation to cognitive deficits and hippocampal changes that are observed in depressive patients.
在本研究中，我们调查了慢性抗抑郁治疗是否能逆转抑郁样社会应激大鼠海马中的突触可塑性变化。为此，将大鼠击败后单独饲养，或进行对照处理后群居。经过至少3个月的一段时间后，大鼠要么长期接受丙咪嗪治疗（20毫克/千克/天，口服至少3个月），要么接受溶剂溶液（即水）治疗。然后，在体外测量海马CA1区的长时程增强和长时程抑制。慢性丙咪嗪治疗部分恢复了社会应激大鼠中减弱的长时程增强诱导，并抑制了长时程抑制诱导的易化。结合在抑郁症患者中观察到的认知缺陷和海马变化，讨论了社会应激后改变的突触可塑性。
