MODULATION OF AN NCAM-RELATED ADHESION MOLECULE WITH LONG-TERM SYNAPTIC PLASTICITY IN APLYSIA

MODULATION OF AN NCAM-RELATED ADHESION MOLECULE WITH LONG-TERM SYNAPTIC PLASTICITY IN APLYSIA
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DOI:
10.1126/science.1585176
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发表时间:
1992-05-01
期刊:
影响因子:
56.9
通讯作者:
KANDEL, ER
KANDEL, ER
中科院分区:
综合性期刊1区
文献类型:
--
作者:
MAYFORD, M;BARZILAI, A;KANDEL, ER

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在海洋软体动物中的一种学习形式,鳃和虹吸管撤回反射的长期敏化,导致突触前虹吸感觉神经元和它们的靶细胞之间形成新的突触连接。当细胞保持在培养物中时,可以通过应用血清素(一种内源性促进性神经递质)来模拟这些结构变化。一组细胞表面蛋白,命名为细胞粘附分子(apCAM)的下调在感觉神经元中对5-羟色胺的反应。从互补DNA克隆获得的推导的氨基酸序列表明,apCAM是一个蛋白质家族,似乎来自一个单一的基因。apCAM是免疫球蛋白类细胞粘附分子的成员,类似于两种神经细胞粘附分子,NCAM和成束蛋白II。除了调节新合成的apCAM外,5-羟色胺还改变了突触前感觉神经元细胞表面上预先存在的apCAM的量。相比之下,突触后运动神经元表面的apCAM不受5-羟色胺的调节。这种快速的,递质介导的下调的感觉神经元中的细胞粘附分子可能是长期突触易化的早期分子变化之一。
A form of learning in the marine mollusk Aplysia, long-term sensitization of the gill- and siphon-withdrawal reflex, results in the formation of new synaptic connections between the presynaptic siphon sensory neurons and their target cells. These structural changes can be mimicked, when the cells are maintained in culture, by application of serotonin, an endogenous facilitating neurotransmitter in Aplysia. A group of cell surface proteins, designated Aplysia cell adhesion molecules (apCAM's) was down-regulated in the sensory neurons in response to serotonin. The deduced amino acid sequence obtained from complementary DNA clones indicated that the apCAM's are a family of proteins that seem to arise from a single gene. The apCAM's are members of the immunoglobulin class of cell adhesion molecules and resemble two neural cell adhesion molecules, NCAM and fasciclin II. In addition to regulating newly synthesized apCAM, serotonin also altered the amount of preexisting apCAM on the cell surface of the presynaptic sensory neurons. By contrast, the apCAM on the surface of the postsynaptic motor neuron was not modulated by serotonin. This rapid, transmitter-mediated down-regulation of a cell adhesion molecule in the sensory neurons may be one of the early molecular changes in long-term synaptic facilitation.