Aplysia cell adhesion molecule and a novel protein kinase C activity in the postsynaptic neuron are required for presynaptic growth and initial formation of specific synapses.

Aplysia cell adhesion molecule and a novel protein kinase C activity in the postsynaptic neuron are required for presynaptic growth and initial formation of specific synapses.
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DOI:
10.1523/jneurosci.0546-10.2010
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发表时间:
2010-06-23
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
通讯作者:
Schacher S
Schacher S
中科院分区:
其他
文献类型:
--
作者:
Hu JY;Chen Y;Bougie JK;Sossin WS;Schacher S

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为了探讨在与特定的突触后靶点(L7而非L11)的感觉神经元突触的初始形成中,失智症细胞粘附分子(ApCAM)和特定蛋白激酶C(PKC)亚型的活性的作用,我们检查了突触前生长、初始突触形成和突触前神经肽sensorin在ApCAM或新型PKC活性的细胞特异性降低后的表达。感觉神经元和L7之间的突触形成在铺板后3小时开始,并伴随着一种新的PKC快速积累到突触相互作用的位点。减少ApCAM的表达,特别是从表面的L7块突触前生长和初始突触的形成,目标诱导的感觉神经元细胞体中的感觉蛋白的增加和快速积累的新的PKC的网站的相互作用。选择性阻断L7中的新型PKC活性,但不阻断感觉神经元中的新型PKC活性,注射干扰新型PKC活性的显性负性构建体,产生与下调ApCAM相同的作用;阻断突触前生长和初始突触形成,以及靶向诱导感觉神经元细胞体中感觉蛋白的增加。结果表明,信号启动突触后细胞粘附分子ApCAM加上一种新的PKC在适当的突触后神经元的激活产生突触前生长所需的逆行信号与初始突触形成,和目标诱导的表达突触前神经肽的突触成熟的关键。
To explore the role of both Aplysia cell adhesion molecule (ApCAM) and activity of specific protein kinase C (PKC) isoforms in the initial formation of sensory neuron synapses with specific postsynaptic targets (L7 but not L11), we examined presynaptic growth, initial synapse formation, and the expression of the presynaptic neuropeptide sensorin following cell-specific reduction of ApCAM or of a novel PKC activity. Synapse formation between sensory neurons and L7 begins by 3 h after plating and is accompanied by a rapid accumulation of a novel PKC to sites of synaptic interaction. Reducing ApCAM expression specifically from the surface of L7 blocks presynaptic growth and initial synapse formation, target-induced increase of sensorin in sensory neuron cell bodies and the rapid accumulation of the novel PKC to sites of interaction. Selective blockade of the novel PKC activity in L7, but not in sensory neurons, with injection of a dominant negative construct that interferes with the novel PKC activity, produces the same actions as down regulating ApCAM; blockade of presynaptic growth and initial synapse formation, and the target-induced increase of sensorin in sensory neuron cell bodies. The results indicate that signals initiated by postsynaptic cell adhesion molecule ApCAM coupled with the activation of a novel PKC in the appropriate postsynaptic neuron produce the retrograde signals required for presynaptic growth associated with initial synapse formation, and the target-induced expression of a presynaptic neuropeptide critical for synapse maturation.