Stabel J, Wisskirchen T, Heinemann U
Institut für Neurophysiologie, Zentrum Physiologie und Pathophysiologie, Universität zu Köln, Cologne, F.R.G.
Brain Res. 1990 Jun 18;520(1-2):215-21. doi: 10.1016/0006-8993(90)91708-o.
Since plastic changes in neuronal tissue are often associated with changes in responses to excitatory amino acids (EAA), a method is required which permits mapping of functional EAA receptor sites. In this study the measurement of extracellular sodium concentration changes [( Na+]o) induced by iontophoretic application of N-methyl-D-aspartate (NMDA) and quisqualate (Quis) is used as a tool to estimate the density of functional NMDA- and Quis-receptor sites in area CA1 and dentate gyrus of rat hippocampus. Largest decreases of [Na+]o induced by NMDA were found in basal and apical dendritic fields of area CA1 and in stratum moleculare of dentate gyrus at a distance of 50-100 microns from stratum granulare. Peak decreases in [Na+]o induced by Quis occurred at similar positions. Bath application of tetrodotoxin (TTX) suppressed that part of the extracellular Na+ loss mediated by Na+ fluxes through voltage activated Na+ channels. However, the laminar profiles of Quis- and NMDA-induced [Na+]o changes were not affected by TTX. Thus, EAA induced decreases in [Na+]o can be used to detect changes in receptor density and in receptor functionality of hippocampus which had undergone plastic changes.
由于神经组织中的可塑性变化通常与对兴奋性氨基酸（EAA）的反应变化相关，因此需要一种方法来绘制功能性EAA受体位点。在本研究中，通过离子电泳应用N-甲基-D-天冬氨酸（NMDA）和quisqualate（Quis）诱导的细胞外钠浓度变化[（Na +）o]的测量被用作估计大鼠海马CA1区和齿状回中功能性NMDA和Quis受体位点密度的工具。在CA1区的基底和顶端树突场以及距颗粒层50-100微米距离的齿状回分子层中发现了由NMDA诱导的[Na +] o的最大降低。由Quis诱导的[Na +] o的峰值降低发生在相似的位置。浴应用河豚毒素（TTX）抑制了由Na +通过电压激活的Na +通道通量介导的细胞外Na +损失的一部分。然而，Quis和NMDA诱导的[Na +] o变化的层状分布不受TTX影响。因此，EAA诱导的[Na +] o降低可用于检测经历可塑性变化的海马体中受体密度和受体功能的变化。
