心理学报
心理學報
심이학보
Acta Psychologica Sinica
2012年
4期
459~468
,共null页
池少鹏 戚智 姬广聚 邝雪莹 林文娟
池少鵬 慼智 姬廣聚 鄺雪瑩 林文娟
지소붕 척지 희엄취 광설형 림문연
脂多糖 抑郁样行为 海马神经细胞 电压依赖钾通道
脂多糖 抑鬱樣行為 海馬神經細胞 電壓依賴鉀通道
지다당 억욱양행위 해마신경세포 전압의뢰갑통도
lipopolysaccharide; depressive-like behavior; hippocampal neuron; voltage-dependent potassiumchannel
采用细胞因子刺激剂脂多糖(lipopolysaccharide,LPS)为免疫激活手段,研究LPS诱导的免疫激活产生的抑郁样行为及对海马神经细胞电压依赖钾电流变化的影响。应用膜片钳技术对海马神经细胞钾电流进行全细胞记录,比较抑郁样行为大鼠与正常大鼠钾离子通道电流密度和激活特性的变化。结果发现,与生理盐水对照组相比,一次LPS注射后2hr,实验组动物产生抑郁样行为,同时急性观察的海马神经细胞的钾离子通道的电流密度呈现显著升高(P〈0.01);而一次LPS注射后24hr,动物的抑郁样行为消失,且急性观察的海马神经细胞的钾离子通道与对照组相比较,其电流密度和激活曲线没有显著性变化。结论:LPS诱导的抑郁样行为,与LPS诱导的海马神经细胞电压依赖钾电流的上调在时程上同步,提示钾离子通道可能参与免疫激活所致的抑郁样行为。
採用細胞因子刺激劑脂多糖(lipopolysaccharide,LPS)為免疫激活手段,研究LPS誘導的免疫激活產生的抑鬱樣行為及對海馬神經細胞電壓依賴鉀電流變化的影響。應用膜片鉗技術對海馬神經細胞鉀電流進行全細胞記錄,比較抑鬱樣行為大鼠與正常大鼠鉀離子通道電流密度和激活特性的變化。結果髮現,與生理鹽水對照組相比,一次LPS註射後2hr,實驗組動物產生抑鬱樣行為,同時急性觀察的海馬神經細胞的鉀離子通道的電流密度呈現顯著升高(P〈0.01);而一次LPS註射後24hr,動物的抑鬱樣行為消失,且急性觀察的海馬神經細胞的鉀離子通道與對照組相比較,其電流密度和激活麯線沒有顯著性變化。結論:LPS誘導的抑鬱樣行為,與LPS誘導的海馬神經細胞電壓依賴鉀電流的上調在時程上同步,提示鉀離子通道可能參與免疫激活所緻的抑鬱樣行為。
채용세포인자자격제지다당(lipopolysaccharide,LPS)위면역격활수단,연구LPS유도적면역격활산생적억욱양행위급대해마신경세포전압의뢰갑전류변화적영향。응용막편겸기술대해마신경세포갑전류진행전세포기록,비교억욱양행위대서여정상대서갑리자통도전류밀도화격활특성적변화。결과발현,여생리염수대조조상비,일차LPS주사후2hr,실험조동물산생억욱양행위,동시급성관찰적해마신경세포적갑리자통도적전류밀도정현현저승고(P〈0.01);이일차LPS주사후24hr,동물적억욱양행위소실,차급성관찰적해마신경세포적갑리자통도여대조조상비교,기전류밀도화격활곡선몰유현저성변화。결론:LPS유도적억욱양행위,여LPS유도적해마신경세포전압의뢰갑전류적상조재시정상동보,제시갑리자통도가능삼여면역격활소치적억욱양행위。
Lipopolysaccharide (LPS)-induced immunity activation can result in evident depressive-like behavior, such as anhedonia and reduced locomotion. Earlier studies have shown that K+ channels, such as Kv7 and TREK-1, are involved in the development of depressive-like behavior in animal models. In the present study, we show that LPS (200 μg/kg) could induce significant short-term depressive-like behavior in rat. In order to get insight into the underlying molecular mechanism, we investigated the potential involvement of rat hippocampal neuron voltage-dependent K+ channels in the depressive-like behaviors induced by LPS. Methods: Twenty rats were randomly divided into LPS and control groups, each with ten rats. The rats in the LPS group were injected with LPS (200 ~tg/kg), while saline was injected in the rats of the control group. The saccharin preference test and open field test were carried out 2 hours and 24 hours after injection of LPS to assess short-term or long-term effects on animal behavior, respectively. Next, 12 rats were randomly divided into LPS 2 hr, LPS 24 hr and control groups, each with four rats for assessing the effect of LPS on K+ channel currents of hippocampal neurons by using whole-cell patch-clamp configuration. Results: The data showed that LPS induced depressive-like behavior in rat after 2 hours of single injection. However, this depressive-like behavior was recovered after 24 hours of single LPS injection. In agreement with these behavioral observations, voltage-dependent K+ current density was increased in neurons isolated from rat after 2 hours of single LPS injection, whereas no significant change was found after 24 hours injection. Conclusion: Our results demonstrate that LPS-induced immunity activation can result in evident short term depressive-like behavior in rats, which are coincident with LPS induced up-regulation of voltage-dependent K+ current in rat hippocampal neurons. This result suggests that voltage-dependent K+ current might contribute to the development of the depressive-like behavior induced by LPS.