摘要
目的:研究孕期维生素A边缘缺乏(MVAD)对仔鼠海马长时程增强的直接影响。方法:将6只健康雌性Wistar大鼠随机分为MVAD和对照组,从交配前3w开始分别饲予维生素A(VA)缺乏饲料(含VA400IU/kg)和VA充足饲料(含VA6500IU/kg)。仔鼠断乳后,继续饲予与其母鼠相同的特殊饲料至生后7w。高效液相技术检测血清VA浓度,运用电生理技术测试7w龄幼鼠海马脑片的长时程增强(LTP),电镜观察海马脑片突触的形态学改变。结果:MVAD组孕鼠及仔鼠血清VA浓度均显著低于对照组;MVAD7w龄幼鼠海马脑片诱发LTP,场兴奋性突触后电位(fEPSP)斜率增加的百分比(25.4±2.01)%明显低于对照组[(57.5%±8.63)%,P<0.01]。MVAD组孵育脑片的人工脑脊液中加入视黄酸(RA)后,fEPSP斜率的改变明显增大(P<0.01),加入铁剂或锌剂后fEPSP斜率的改变没有显著差异(P>0.05)。对照组孵育脑片的人工脑脊液中加入RA受体拮抗剂(Ro41-5253)后,fEPSP斜率的改变明显减小;电镜观察,强直刺激后1h,脑脊液中补充RA的比没有补充RA的MVAD组脑片的突触界面曲率增大。结论:孕期VA边缘缺乏能直接损害幼鼠海马的LTP。
Objective. To study the effects of marginal vitamin A deficiency (MVAD) on the hippocampal CA1 long-term potentiation (LTP) in young rats. Methods. Six female rats were divided into two groups at random, three in MVAD group, three in control group. The rats were fed VA deficient diet (400IU VA/kg) and VA sufficient diet (6 500IU VA/kg) respectively since 3 w before coitus. Serum VA was assessed by high performance liquid chromatography (HPLC). The young rats were killed at D49. The hippocampal CA1 LTP was detected by electrophysiological technique and the ultrastructure of synapses was observed by electron microscope, Results.. The changes of field excitatory postsynaptic potentials (fEPSP) slope (25.4%±2.01%) in MVAD young rats aged 7 weeks were much lower than that in control group (57.5%±8.63%). The changes of slope of fEPSP induced by MVAD in young rats could be replenished after adding retinoic acid (P〈0.01), However, LTP impairment was re-observed after adding RA antagonist,Ro41-5253 in control group (P〈0.01). No differences of LTP were found after adding FeSO4 or ZnSO4 (P〉0.05). The curvature in synaptic interface of MVAD group was less than that of the MVAD supplemented RA group and the control. Conclusion: MVAD during embryonic and early postnatal period can directly impair the hippocampal CA1 LTP of young rats. [ACTA NUTRIMENTA SINICA, 2006, 28(1): 32-
35]
出处
《营养学报》
CAS
CSCD
北大核心
2006年第1期32-35,共4页
Acta Nutrimenta Sinica
基金
国家自然科学基金(No.30471462)
关键词
维生素A
幼鼠
海马
长时程增强
vitaminA deficiency
young rat
hippocampus
LTP