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动作电位非依赖性微小神经传递对突触缩放的调节。

Regulation of synaptic scaling by action potential-independent miniature neurotransmission.

机构信息

Physiology Department, Emory University, School of Medicine, Atlanta, Georgia.

Doctorado en Ciencias Biológicas, Univerisdad Autónoma de Tlaxcala, Tlaxcala, Mexico.

出版信息

J Neurosci Res. 2018 Mar;96(3):348-353. doi: 10.1002/jnr.24138. Epub 2017 Aug 7.

Abstract

Synaptic scaling represents a homeostatic adjustment in synaptic strength that was first identified as a cell-wide mechanism to achieve firing rate homeostasis after perturbations to spiking activity levels. In this review, we consider a form of synaptic scaling that is triggered by changes in action potential-independent neurotransmitter release. This plasticity appears to be both triggered and expressed locally at the dendritic site of the synapse that experiences a perturbation. A discussion of different forms of scaling triggered by different perturbations is presented. We consider work from multiple groups supporting this form of scaling, which we call neurotransmission-based scaling. This class of homeostatic synaptic plasticity is compared in studies using hippocampal and cortical cultures, as well as in vivo work in the embryonic chick spinal cord. Despite differences in the tissues examined, there are clear similarities in neurotransmission-based scaling, which appear to be molecularly distinct from the originally described spike-based scaling.

摘要

突触可塑性代表了突触强度的一种自身稳态调节,最初被确定为一种在尖峰活动水平受到干扰后实现放电率自身稳态的全细胞机制。在这篇综述中,我们考虑了一种由动作电位非依赖性神经递质释放变化引发的突触可塑性。这种可塑性似乎在经历干扰的突触树突部位被局部触发和表达。本文讨论了由不同的扰动触发的不同形式的可塑性。我们考虑了多个支持这种可塑性的小组的工作,我们称之为基于神经传递的可塑性。这种类型的自身稳态突触可塑性在使用海马体和皮层培养物的研究中以及在胚胎鸡脊髓的体内研究中进行了比较。尽管所检查的组织存在差异,但基于神经传递的可塑性存在明显的相似之处,它在分子上与最初描述的基于尖峰的可塑性明显不同。

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