Activity affects dendritic shape and synapse elimination during steroid controlled dendritic retraction in Manduca sexta
Activity affects dendritic shape and synapse elimination during steroid controlled dendritic retraction in Manduca sexta
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DOI：
10.1523/jneurosci.3189-04.2004
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发表时间：
2004-11-03
影响因子：
5.3
通讯作者：
Mentel, T
中科院分区：
文献类型：
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作者：
Duch, C;Mentel, T
昆虫变态是树突和突触重塑的一个引人注目的例子，幼虫和成虫的行为对中枢神经系统有不同的要求。在蛾的变态过程中，Manduca sexta，许多幼虫运动神经元被重塑，以在成虫中发挥新的功能。在幼虫生命的后期，类固醇激素触发轴突和树突退化以及幼虫突触消除。这些退化事件伴随着所谓的徘徊阶段期间运动行为的刻板变化。两个正常发生的树突形状和运动输出的变化，以前已经进行了定量分析的个别识别的运动神经元MN5。本研究通过长期植入细胞外电极测试活动是否影响MN5中类固醇诱导的树突消退和突触解体。在发育期间，在正常发育的完整动物体内刺激MN5，当它通常不显示活性时，显着减缓了高阶树突的消退。生理和解剖分析表明，减少树突回归伴随着幼虫突触拆卸显着减少。因此，类固醇诱导的树突形状和突触连接的改变是由活性依赖性机制修饰的。这种相互作用可能是快速调整僵硬，不灵活的荷尔蒙程序的常见机制。
Insect metamorphosis is a compelling example for dendritic and synaptic remodeling as larval and adult behaviors place distinct demands on the CNS. During the metamorphosis of the moth, Manduca sexta, many larval motoneurons are remodeled to serve a new function in the adult. During late larval life, steroid hormones trigger axonal and dendritic regression as well as larval synapse elimination. These regressive events are accompanied by stereotypical changes in motor behavior during the so-called wandering stages. Both normally occurring changes in dendritic shape and in motor output have previously been analyzed quantitatively for the individually identified motoneuron MN5. This study tested whether activity affected steroid-induced dendritic regression and synapse disassembly in MN5 by means of chronically implanted extracellular electrodes. Stimulating MN5 in vivo in intact, normally developing animals during a developmental period when it usually shows no activity significantly slowed the regression of high-order dendrites. Both physiological and anatomical analysis demonstrated that reduced dendritic regression was accompanied by a significant reduction in larval synapse disassembly. Therefore, steroid-induced alterations of dendritic shape and synaptic connectivity are modified by activity-dependent mechanisms. This interaction might be a common mechanism for rapid adjustments of rigid, inflexible, hormonal programs.