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营养分子与神经系统的进化

Trophic molecules and evolution of the nervous system.

作者信息

Black I B

出版信息

Proc Natl Acad Sci U S A. 1986 Nov;83(21):8249-52. doi: 10.1073/pnas.83.21.8249.

DOI:10.1073/pnas.83.21.8249
PMID:3022286
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC386905/
Abstract

Although recent work has reemphasized the general importance of ontogeny in evolution, underlying developmental molecular mechanisms are largely undefined. What heritable ontogenetic mechanisms result in the evolution of new morphologies and functions? Such questions are particularly difficult in the nervous system, in which each of 10(11) neurons forms approximately equal to 10(4) specific interconnections. I propose that specific heritable, trophic interactions during development, which determine cell survival and pathway size, form a substrate for neural evolution. This model is based on the observation that neurons are vastly overproduced during ontogeny; neurons, their pathways and connections are dependent on target-derived trophic factors for developmental survival; and co-innervating, functionally and anatomically distinct neural populations compete for common trophic factors for survival. Focusing on sympathetic and sensory neurons, which require the target-derived, trophic protein nerve growth factor at different times for developmental survival, and which innervate common targets, different classes of ontogenetic evolutionary mechanisms may be characterized. Evolution may occur from heritable changes in the structure of trophic gene products or altered timing of expression. Molecular mechanisms underlying heterochrony are thereby described. The model is directly applicable to evolution of the brain and is testable in a variety of situations.

摘要

尽管最近的研究再次强调了个体发育在进化中的普遍重要性,但潜在的发育分子机制在很大程度上仍不明确。哪些可遗传的个体发育机制导致了新形态和功能的进化?这类问题在神经系统中尤其困难,因为在神经系统中,10¹¹个神经元中的每一个都形成了大约10⁴个特定的相互连接。我提出,发育过程中特定的、可遗传的营养相互作用决定了细胞存活和通路大小,构成了神经进化的基础。该模型基于以下观察结果:神经元在个体发育过程中大量过剩;神经元、它们的通路和连接依赖于靶源性营养因子来维持发育存活;共同支配、功能和解剖结构不同的神经群体竞争共同的营养因子以维持存活。以交感神经元和感觉神经元为例,它们在发育存活的不同时间需要靶源性营养蛋白神经生长因子,并且支配共同的靶标,可以对不同类别的个体发育进化机制进行表征。进化可能源于营养基因产物结构的可遗传变化或表达时间的改变。由此描述了异时性的分子机制。该模型可直接应用于大脑的进化,并在多种情况下可进行检验。

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引用本文的文献

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When Nerve Growth Factor Met Behavior.当神经生长因子遇见行为时。
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2
NGF, brain and behavioral plasticity.神经生长因子、大脑和行为可塑性。
Neural Plast. 2012;2012:784040. doi: 10.1155/2012/784040. Epub 2012 Feb 16.
3
Molecular cloning and neurotrophic activities of a protein with structural similarities to nerve growth factor: developmental and topographical expression in the brain.一种与神经生长因子结构相似的蛋白质的分子克隆及神经营养活性:在脑中的发育及局部表达
Proc Natl Acad Sci U S A. 1990 Jul;87(14):5454-8. doi: 10.1073/pnas.87.14.5454.
4
Depolarizing stimuli regulate nerve growth factor gene expression in cultured hippocampal neurons.去极化刺激调节培养海马神经元中神经生长因子基因的表达。
Proc Natl Acad Sci U S A. 1991 Jul 15;88(14):6289-92. doi: 10.1073/pnas.88.14.6289.
5
Plasticity in expression of calcitonin gene-related peptide and substance P immunoreactivity in ganglia and fibres following guanethidine and/or capsaicin denervation.胍乙啶和/或辣椒素去神经支配后神经节和纤维中降钙素基因相关肽和P物质免疫反应性表达的可塑性。
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本文引用的文献

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Ontophyletics of the nervous system: eyeless mutants illustrate how ontogenetic buffer mechanisms channel evolution.神经系统的个体发生系统发育:无眼突变体说明了个体发生缓冲机制如何引导进化。
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