Triana-Baltzer Gallen B, Liu Zhaoping, Gounko Natalia V, Berg Darwin K
Neurobiology Section, Division of Biological Sciences, 0357, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0357, USA.
Mol Cell Neurosci. 2008 Sep;39(1):74-82. doi: 10.1016/j.mcn.2008.05.017. Epub 2008 Jun 4.
Neuroligin, SynCAM, and L1-CAM are cell adhesion molecules with synaptogenic roles in glutamatergic pathways. We show here that SynCAM is expressed in the chick ciliary ganglion, embedded in a nicotinic pathway, and, as shown previously for neuroligin and L1-CAM, acts transcellularly to promote synaptic maturation on the neurons in culture. Moreover, we show that electroporation of chick embryos with dominant negative constructs disrupting any of the three molecules in vivo reduces the total amount of presynaptic SV2 overlaying the neurons expressing the constructs. Only disruption of L1-CAM and neuroligin, however, reduces the number of SV2 puncta specifically overlaying nicotinic receptor clusters. Disrupting L1-CAM and neuroligin together produces no additional decrement, indicating that they act on the same subset of synapses. SynCAM may affect synaptic maturation rather than synapse formation. The results indicate that individual neurons can express multiple synaptogenic molecules with different effects on the same class of nicotinic synapses.
神经连接蛋白、突触细胞粘附分子（SynCAM）和L1细胞粘附分子（L1-CAM）是在谷氨酸能通路中具有突触生成作用的细胞粘附分子。我们在此表明，SynCAM在鸡睫状神经节中表达，该神经节嵌入烟碱能通路，并且，如先前对神经连接蛋白和L1-CAM的研究所示，它通过跨细胞作用促进培养中的神经元上的突触成熟。此外，我们表明，用显性负性构建体对鸡胚进行电穿孔，在体内破坏这三种分子中的任何一种，都会减少覆盖表达构建体的神经元的突触前突触囊泡蛋白2（SV2）的总量。然而，只有破坏L1-CAM和神经连接蛋白，才会减少特异性覆盖烟碱受体簇的SV2斑点的数量。同时破坏L1-CAM和神经连接蛋白不会产生额外的减少，这表明它们作用于同一子集的突触。SynCAM可能影响突触成熟而非突触形成。结果表明，单个神经元可以表达多种对同一类烟碱能突触具有不同作用的突触生成分子。
