Lüthi A, Laurent J P, Figurov A, Muller D, Schachner M
Pharma Division, Preclinical Research, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
Nature. 1994;372(6508):777-9. doi: 10.1038/372777a0.
Synaptic membranes express cell adhesion molecules. Here we investigate the role of the neural cell adhesion molecules L1 and NCAM in hippocampal long-term potentiation (LTP), a sustained-use-dependent increase in synaptic efficacy that has been implicated in learning and memory. L1 and NCAM mediate cell interactions during neural development and are strongly expressed in the hippocampus. They cooperate to strengthen L1-dependent cell adhesion and are coupled to second messenger pathways. We show that LTP in CA1 neurons of rat hippocampal slices was reduced by application of various L1 and NCAM antibodies, recombinant L1 fragments, and upon dissociation of the L1/NCAM complex through oligomannosidic carbohydrates and NCAM peptides. Neither the activation of NMDA (N-methyl-D-aspartate) receptors nor the maintenance of LTP was affected. These results suggest that L1 and NCAM modulate the development or the stabilization of LTP.
突触膜表达细胞黏附分子。在此，我们研究神经细胞黏附分子L1和NCAM在海马体长期增强（LTP）中的作用，LTP是一种持续使用依赖的突触效能增加，与学习和记忆有关。L1和NCAM在神经发育过程中介导细胞间相互作用，且在海马体中大量表达。它们协同增强依赖L1的细胞黏附，并与第二信使途径相偶联。我们发现，应用各种L1和NCAM抗体、重组L1片段，以及通过低聚甘露糖碳水化合物和NCAM肽解离L1/NCAM复合物后，大鼠海马体切片CA1神经元中的LTP降低。NMDA（N-甲基-D-天冬氨酸）受体的激活和LTP的维持均未受影响。这些结果表明，L1和NCAM调节LTP的形成或稳定。
