我们的研究基于鸡成分化软骨细胞和健康、病理人类色素细胞的N-甲基-D-天门冬氨酸型谷氨酸受体研究。鉴于NMDAR主要介导Ca2+电流，我们侧重于Ca2+稳态的变化。实验证明，NMDAR可能在软骨祖细胞内精确调节的细胞内Ca2+振荡中发挥作用，并且NMDAR诱导的Ca2+信号与最佳软骨发生关联。在涉及亚细胞分数的黑色素瘤细胞中的NMDAR亚基蛋白表达情况揭示了黑色素细胞和黑色素瘤细胞之间的重大差异，后者可能存在功能核NMDAR。总之，我们首次在非神经系统外的非可兴奋细胞中，通过体外实验证明了功能性NMDAR的存在（在成分化软骨细胞中），以及NMDAR的核定位（在黑色素瘤细胞中）。前者介导了在软骨发生中不可或缺的Ca2+-依赖性途径，而后者可能是由于恶性转化而形成的。

Our research was based on studies involving N-methyl- D-aspartate type glutamate receptors in chicken-derived differentiating chondrocytes, as well as in healthy and pathological human pigment cells. Given that NMDARs primarily mediate Ca2+ currents, we focused on the changes of Ca2+ homeostasis. The experiments proved that NMDARs may have roles in the precisely regulated intracellular Ca2+ oscillations of chondroprogenitor cells, and NMDAR-evoked Ca2+ signals are associated with optimal chondrogenesis. NMDAR subunit protein expression profiles in melanoma cells, involving subcellular fractions, revealed major differences between melanocytes and melanoma cells with potentially functional nuclear NMDARs in the latter. In summary we demonstrated in vitro, for the first time, in non-excitable cells from outside the nervous system the presence of functional NMDARs (in differentiating chondrocytes), and the nuclear localisation of NMDARs (in melanoma cells). The former mediate Ca2+-dependent pathways that are indispensable to chondrogenesis, while the latter may have appeared as a result of malignant transformation.