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Restoration of ocular dominance plasticity mediated by adenosine 3',5'-monophosphate in adult visual cortex.成年视觉皮层中由3',5'-单磷酸腺苷介导的眼优势可塑性的恢复。
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果蝇轴突生长的环境依赖性可塑性中的神经元活动与腺苷酸环化酶

Neuronal activity and adenylyl cyclase in environment-dependent plasticity of axonal outgrowth in Drosophila.

作者信息

Zhong Yi, Wu Chun-Fang

机构信息

Department Biological Sciences, University of Iowa, Iowa City, Iowa 52242, USA.

出版信息

J Neurosci. 2004 Feb 11;24(6):1439-45. doi: 10.1523/JNEUROSCI.0740-02.2004.

DOI:10.1523/JNEUROSCI.0740-02.2004
PMID:14960616
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1289273/
Abstract

The development of the nervous system is influenced by environmental factors. Among all environmental factors, temperature belongs to a unique category. Besides activating some specific sensory pathways, it exerts nonspecific, pervasive effects directly on the entire nervous system, especially in exothermic species. This study uses mutants to genetically discover how temperature affects nerve terminal arborization at larval neuromuscular junctions of Drosophila. It is known that hyperexcitability in K(+) channel mutants leads to enhanced ramification of larval nerve terminals. Elevated cAMP levels in dunce mutants with reduced phosphodiesterase activity also cause enhanced arborization. These genetic alterations are thought to perturb mechanisms relevant to activity-dependent neural plasticity, in which neuronal activity activates the cAMP pathway, and consequently affect nerve terminal arborization by regulating expression of adhesion molecules. Here we demonstrate the robust influence of rearing temperature on motor nerve terminal arborization. Analysis of ion channel and cAMP pathway mutants indicates that this temperature-dependent plasticity is mediated via neuronal activity changes linked to mechanisms controlled by the rutabaga-encoded adenylyl cyclase.

摘要

神经系统的发育受环境因素影响。在所有环境因素中,温度属于独特的一类。除了激活一些特定的感觉通路外,它还直接对整个神经系统产生非特异性的、广泛的影响,在变温动物中尤其如此。本研究利用突变体从遗传学角度探究温度如何影响果蝇幼虫神经肌肉接头处的神经末梢分支。已知钾离子通道突变体中的过度兴奋会导致幼虫神经末梢分支增多。磷酸二酯酶活性降低的“傻瓜”突变体中升高的环磷酸腺苷(cAMP)水平也会导致分支增多。这些基因改变被认为扰乱了与活动依赖型神经可塑性相关的机制,在该机制中神经元活动激活cAMP通路,进而通过调节黏附分子的表达来影响神经末梢分支。在此我们证明了饲养温度对运动神经末梢分支有强大的影响。对离子通道和cAMP通路突变体的分析表明,这种温度依赖性可塑性是通过与由rutabaga编码的腺苷酸环化酶所控制的机制相关联的神经元活动变化介导的。