精神疾病和神经退行性疾病中突触和树突维持及其破坏的机制。
Mechanisms of synapse and dendrite maintenance and their disruption in psychiatric and neurodegenerative disorders.
机构信息
Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06520-8024, USA.
出版信息
Annu Rev Neurosci. 2010;33:349-78. doi: 10.1146/annurev-neuro-060909-153204.
Emerging evidence indicates that once established, synapses and dendrites can be maintained for long periods, if not for the organism's entire lifetime. In contrast to the wealth of knowledge regarding axon, dendrite, and synapse development, we understand comparatively little about the cellular and molecular mechanisms that enable long-term synapse and dendrite maintenance. Here, we review how the actin cytoskeleton and its regulators, adhesion receptors, and scaffolding proteins mediate synapse and dendrite maintenance. We examine how these mechanisms are reinforced by trophic signals passed between the pre- and postsynaptic compartments. We also discuss how synapse and dendrite maintenance mechanisms are compromised in psychiatric and neurodegenerative disorders.
新出现的证据表明,一旦形成,突触和树突可以长期维持,如果不是整个生物体的生命周期的话。与关于轴突、树突和突触发育的丰富知识相比,我们对能够长期维持突触和树突的细胞和分子机制知之甚少。在这里,我们回顾了肌动蛋白细胞骨架及其调节剂、粘附受体和支架蛋白如何介导突触和树突的维持。我们研究了这些机制如何通过突触前和突触后隔室之间传递的营养信号得到加强。我们还讨论了在精神疾病和神经退行性疾病中,突触和树突维持机制是如何受到损害的。