Suppr超能文献

体外培养时,感觉或运动细胞导致生长锥-神经突束化减少,同时神经递质会下调海兔细胞黏附分子。

Decrease in growth cone-neurite fasciculation by sensory or motor cells in vitro accompanies downregulation of Aplysia cell adhesion molecules by neurotransmitters.

作者信息

Peter N, Aronoff B, Wu F, Schacher S

机构信息

Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, New York.

出版信息

J Neurosci. 1994 Mar;14(3 Pt 2):1413-21. doi: 10.1523/JNEUROSCI.14-03-01413.1994.

Abstract

Cell adhesion molecules play important roles in axon guidance and synapse formation. Recent studies suggest that the expression of some of these molecules can be regulated either by electrical activity or by specific neurotransmitters. The expression of neural cell adhesion molecule (NCAM)-like molecules in Aplysia, designated apCAM, is downregulated from the surface of sensory neurons by 5-HT, a transmitter known to evoke long-term changes in the structure and function of these neurons. We tested whether the distribution of apCAM on the surface of other neurons can be regulated by treatments with other neurotransmitters known to evoke long-term functional and structural changes in Aplysia neurons, and we examined the consequences of treatments with the neurotransmitters on the pattern of growth cone-neurite interactions. We report that applications of the neuropeptide Phe-Met-Arg-Phe-amide (FMRFamide) that evoke long-term synaptic depression also reduce apCAM expression on the surface of motor cell L7 via a mechanism that appears to be similar to the mechanism mediating the 5-HT-induced change in the sensory cells. Specific treatments that affect apCAM distribution on the surface of their respective cells, 5-HT on sensory cells or FMRFamide on motor cell L7, mimic treatment with monoclonal antibodies against apCAM by evoking a significant reduction in the fasciculation of growth cones with other neurites extending from homologous cells.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

细胞黏附分子在轴突导向和突触形成中发挥着重要作用。最近的研究表明,其中一些分子的表达可由电活动或特定神经递质调控。海兔中神经细胞黏附分子(NCAM)样分子(称为apCAM)的表达,会被5-羟色胺(一种已知能引起这些神经元结构和功能长期变化的递质)从感觉神经元表面下调。我们测试了apCAM在其他神经元表面的分布是否能被已知可引起海兔神经元长期功能和结构变化的其他神经递质处理所调控,并且我们研究了用这些神经递质处理对生长锥 - 神经突相互作用模式的影响。我们报告称,能引起长期突触抑制的神经肽苯丙氨酸 - 甲硫氨酸 - 精氨酸 - 苯丙氨酸酰胺(FMRF酰胺)的应用,也会通过一种似乎与介导感觉细胞中5-羟色胺诱导变化的机制相似的机制,降低运动细胞L7表面的apCAM表达。影响apCAM在其各自细胞表面分布的特定处理,即感觉细胞上的5-羟色胺或运动细胞L7上的FMRF酰胺,通过引起生长锥与从同源细胞延伸出的其他神经突的束状化显著减少,模拟了用抗apCAM单克隆抗体的处理。(摘要截选至250字)

相似文献

引用本文的文献

4
Polysialic acid and activity-dependent synapse remodeling.聚唾液酸与活性依赖的突触重塑。
Cell Adh Migr. 2009 Jan-Mar;3(1):43-50. doi: 10.4161/cam.3.1.7258. Epub 2009 Jan 23.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验