Sanabria E R G, Pereira M F S, Dolnikoff M S, Andrade I S, Ferreira A T, Cavalheiro E A, Fernandes M J S
Departamento de Neurologia e Neurocirurgia, Disciplina de Neurologia Experimental, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, SP, Brazil.
Brain Res Bull. 2002 Oct 15;59(1):47-51. doi: 10.1016/s0361-9230(02)00837-7.
Rats subjected to monosodium glutamate (MSG) administration during the neonatal period present chronic neuroendocrine dysfunction associated with marked cognitive deficits. Long-term potentiation (LTP) in the hippocampus provides a model suited for the study of mammalian brain plasticity and memory formation. In the present work, we used the LTP protocol to investigate the synaptic plasticity in the hippocampal CA1 area of adult rats subjected to MSG treatment during the first 10 days of life. Synaptic transmission in CA1 area was analyzed using extracellular field recordings in response to Schaffer's collateral fiber stimulation in hippocampal slices. Animals injected with MSG exhibited a dramatic decrement of LTP field excitatory postsynaptic potentials (fEPSPs) compared to control group. Analysis of percent enhancement of fEPSP slope at 2 min after high frequency stimulation (HFS) increased by 189.3 +/- 33.2% in slices from control rats and 129.45 +/- 18.5% (p < 0.01) in slices from MSG-treated rats. Additionally, MSG-treated animals failed to maintain or consolidate LTP as revealed by a significant reduction in fEPSP slope enhancement over time after HFS. The mean fEPSP slope, 60 min after HFS, was 154.28 +/- 21% of the average baseline slope in control slices versus only 124.4 +/- 15% in MSG-treated rats (p < 0.01). At 90 min after HFS, slices from controls reached a potentiation of 44.5 +/- 2.9%, whereas the MSG group displayed an overall response enhancement of 17.65 +/- 2.7% of basal levels (p < 0.01). These findings indicate that MSG-treated rats display a chronic impairment of CA1 synaptic plasticity.
在新生期接受味精（MSG）给药的大鼠表现出与明显认知缺陷相关的慢性神经内分泌功能障碍。海马体中的长时程增强（LTP）为研究哺乳动物大脑可塑性和记忆形成提供了一个合适的模型。在本研究中，我们使用LTP方案来研究在生命的前10天接受MSG治疗的成年大鼠海马CA1区的突触可塑性。使用细胞外场记录分析CA1区的突触传递，以响应海马切片中施万细胞侧支纤维刺激。与对照组相比，注射MSG的动物的LTP场兴奋性突触后电位（fEPSP）显著降低。高频刺激（HFS）后2分钟fEPSP斜率增强百分比的分析显示，对照组大鼠切片中增加了189.3±33.2%，而MSG处理组大鼠切片中增加了129.45±18.5%（p<0.01）。此外，如HFS后随时间fEPSP斜率增强的显著降低所示，MSG处理的动物未能维持或巩固LTP。HFS后60分钟，平均fEPSP斜率在对照切片中为平均基线斜率的154.28±21%，而在MSG处理的大鼠中仅为124.4±15%（p<0.01）。HFS后90分钟，对照组切片达到44.5±2.9%的增强，而MSG组显示总体反应增强为基础水平的17.65±2.7%（p<0.01）。这些发现表明，MSG处理的大鼠表现出CA1突触可塑性的慢性损伤。
