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Citalopram prevents sleep-deprivation-induced reduction in CaMKII-CREB-BDNF signaling in mouse prefrontal cortex.
Brain Research Bulletin ( IF 3.5 ) Pub Date : 2019-11-16 , DOI: 10.1016/j.brainresbull.2019.11.007
Afzal Misrani 1 , Sidra Tabassum 1 , Meng Wang 2 , Jian Chen 2 , Li Yang 3 , Cheng Long 4
Affiliation  

Curtailment of sleep in modern society leads to a spectrum of neuropsychiatric disorders. However, the molecular mechanisms underlying the effects of sleep deprivation (SD) remain elusive and currently there is no effective therapy to alleviate these effects. Here, we aimed to examine SD-induced cellular and molecular alterations in mouse prefrontal cortex (PFC) and whether subchronic citalopram (CTM) treatment can negate these alterations. Three-month-old C57BL/6 J mice were divided into control (Ctrl), SD, CTM alone and CTM + SD groups. CTM and CTM + SD group mice were treated with CTM for five consecutive days at a dose of 10 mg/kg per day before the experimental procedure. SD and CTM + SD group mice were sleep-deprived for 24 h using an automated treadmill method. We found that 24 h SD causes a marked reduction in the levels of phosphorylated calcium/calmodulin kinase II (pCaMKII), phosphorylated cyclic AMP-responsive element binding protein (pCREB) and brain-derived neurotrophic factor (BDNF) in mouse PFC. Patch clamp recording of pyramidal neurons from acute PFC slices revealed that SD decreases the amplitude of miniature excitatory postsynaptic currents (mEPSCs), suggesting a SD-induced postsynaptic alteration. Interestingly, subchronic CTM treatment prevents such SD-induced reductions in pCaMKII, pCREB and BDNF levels, and in mEPSC amplitude. These data suggest that CTM offers neuroprotection against SD-induced molecular and electrophysiological alterations.

中文翻译:

西酞普兰可预防小鼠前额叶皮质中睡眠剥夺引起的CaMKII-CREB-BDNF信号传导减少。

在现代社会中减少睡眠会导致一系列神经精神疾病。但是,睡眠剥夺(SD)影响的分子机制仍然难以捉摸,目前尚无有效的疗法可减轻这些影响。在这里,我们旨在检查SD诱导的小鼠前额叶皮层(PFC)中的细胞和分子改变,以及亚慢性西酞普兰(CTM)治疗是否可以消除这些改变。将三个月大的C57BL / 6 J小鼠分为对照组(Ctrl),SD,仅CTM和CTM + SD组。在实验程序之前,将CTM和CTM + SD组小鼠以每天10 mg / kg的剂量连续5天用CTM处理。使用自动跑步机方法将SD和CTM + SD组小鼠睡眠剥夺24小时。我们发现24小时SD会导致小鼠PFC中磷酸化钙/钙调蛋白激酶II(pCaMKII),磷酸化环AMP响应元件结合蛋白(pCREB)和脑源性神经营养因子(BDNF)的水平显着降低。膜片钳记录急性PFC切片的锥体神经元显示,SD降低了小型兴奋性突触后突触电流(mEPSCs)的幅度,表明SD诱导的突触后突触改变。有趣的是,亚慢性CTM治疗可防止SD引起的pCaMKII,pCREB和BDNF水平以及mEPSC幅度的降低。这些数据表明,CTM对SD诱导的分子和电生理改变具有神经保护作用。小鼠PFC中的磷酸化环AMP响应元件结合蛋白(pCREB)和脑源性神经营养因子(BDNF)。膜片钳记录急性PFC切片的锥体神经元显示,SD降低了小型兴奋性突触后突触电流(mEPSCs)的幅度,表明SD诱导的突触后突触改变。有趣的是,亚慢性CTM治疗可防止SD引起的pCaMKII,pCREB和BDNF水平以及mEPSC幅度的降低。这些数据表明,CTM对SD诱导的分子和电生理改变具有神经保护作用。小鼠PFC中的磷酸化环AMP响应元件结合蛋白(pCREB)和脑源性神经营养因子(BDNF)。膜片钳记录急性PFC切片的锥体神经元显示,SD降低了小型兴奋性突触后突触电流(mEPSCs)的幅度,表明SD诱导的突触后突触改变。有趣的是,亚慢性CTM治疗可防止SD引起的pCaMKII,pCREB和BDNF水平以及mEPSC幅度的降低。这些数据表明,CTM对SD诱导的分子和电生理改变具有神经保护作用。亚慢性CTM治疗可防止SD引起的pCaMKII,pCREB和BDNF水平以及mEPSC幅度的降低。这些数据表明,CTM对SD诱导的分子和电生理改变具有神经保护作用。亚慢性CTM治疗可防止SD引起的pCaMKII,pCREB和BDNF水平以及mEPSC幅度的降低。这些数据表明,CTM对SD诱导的分子和电生理改变具有神经保护作用。
更新日期:2019-11-18
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