Mezzera Cecilia, López-Bendito Guillermina
Instituto de Neurociencias de Alicante, Universidad Miguel Hernandez-Consejo Superior de Investigaciones Científicas (UMH-CSIC), Av Ramon y Cajal s/n, San Joan d'Alacant 03550, Alicante, Spain.
J Chem Neuroanat. 2016 Sep;75(Pt A):32-40. doi: 10.1016/j.jchemneu.2015.09.005. Epub 2015 Oct 13.
Over recent decades, our understanding of the plasticity of the central nervous system has expanded enormously. Accordingly, it is now widely accepted that the brain can adapt to changes by reorganizing its circuitry, both in response to external stimuli and experience, as well as through intrinsic mechanisms. A clear example of this is the activation of a deprived sensory area and the expansion of spared sensory cortical regions in individuals who suffered peripheral sensory loss. Despite the efforts to understand these neuroplastic changes, the mechanisms underlying such adaptive remodeling remains poorly understood. Progress in understanding these events may be hindered by the highly varied data obtained from the distinct experimental paradigms analyzed, which include different animal models and neuronal systems, as well as studies into the onset of sensory loss. Here, we will establish the current state-of-the-art describing the principal observations made according to the time of sensory deprivation with respect to the development of the thalamocortical connectivity. We will review the experimental data obtained from animal models where sensory deprivation has been induced either before or after thalamocortical axons reach and invade their target cortical areas. The anatomical and functional effects of sensory loss on the primary sensory areas of the cortex will be presented. Indeed, we consider that the comparative approach of this review is a necessary step in order to help deciphering the processes that underlie sensory neuroplasticity, for which studies in animal models have been indispensable. Understanding these mechanisms will then help to develop restorative strategies and prostheses that will overcome the functional loss.
在最近几十年里,我们对中枢神经系统可塑性的理解有了极大的扩展。因此,现在人们普遍认为,大脑可以通过重新组织其神经回路来适应变化,这既可以对外界刺激和经验做出反应,也可以通过内在机制实现。一个明显的例子是,在遭受外周感觉丧失的个体中,被剥夺的感觉区域会被激活,而未受损的感觉皮层区域会扩大。尽管人们努力去理解这些神经可塑性变化,但其适应性重塑背后的机制仍然知之甚少。从不同实验范式(包括不同动物模型和神经元系统以及对感觉丧失起始的研究)获得的高度多样化数据,可能会阻碍我们对这些事件的理解。在这里,我们将阐述当前的研究现状,描述根据感觉剥夺时间对丘脑皮质连接发育所做的主要观察。我们将回顾从动物模型中获得的实验数据,在这些模型中,感觉剥夺是在丘脑皮质轴突到达并侵入其目标皮质区域之前或之后诱导的。我们将展示感觉丧失对皮层主要感觉区域的解剖学和功能影响。事实上,我们认为本综述的比较方法是帮助解读感觉神经可塑性背后过程的必要步骤,而动物模型研究对此不可或缺。了解这些机制将有助于开发恢复性策略和假体,以克服功能丧失。