Moulin Thiago C, Rayêe Danielle, Schiöth Helgi B
Functional Pharmacology Unit, Department of Neuroscience, Uppsala University, Uppsala, Sweden; Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; Department of Ophthalmology and Visual Sciences, Albert Einstein College of Medicine, NY, USA.
Neural Regen Res. 2022 Jan;17(1):20-24. doi: 10.4103/1673-5374.314283.
Mechanisms of homeostatic plasticity promote compensatory changes of cellular excitability in response to chronic changes in the network activity. This type of plasticity is essential for the maintenance of brain circuits and is involved in the regulation of neural regeneration and the progress of neurodegenerative disorders. One of the most studied homeostatic processes is synaptic scaling, where global synaptic adjustments take place to restore the neuronal firing rate to a physiological range by the modulation of synaptic receptors, neurotransmitters, and morphology. However, despite the comprehensive literature on the electrophysiological properties of homeostatic scaling, less is known about the structural adjustments that occur in the synapses and dendritic tree. In this study, we performed a meta-analysis of articles investigating the effects of chronic network excitation (synaptic downscaling) or inhibition (synaptic upscaling) on the dendritic spine density of neurons. Our results indicate that spine density is consistently reduced after protocols that induce synaptic scaling, independent of the intervention type. Then, we discuss the implication of our findings to the current knowledge on the morphological changes induced by homeostatic plasticity.
稳态可塑性机制促进细胞兴奋性的代偿性变化,以响应网络活动的慢性变化。这种可塑性类型对于脑回路的维持至关重要,并参与神经再生的调节和神经退行性疾病的进展。研究最多的稳态过程之一是突触缩放,即通过调节突触受体、神经递质和形态,进行全局突触调整,以将神经元放电率恢复到生理范围。然而,尽管关于稳态缩放的电生理特性已有大量文献,但对于突触和树突棘中发生的结构调整却知之甚少。在本研究中,我们对研究慢性网络兴奋(突触缩小)或抑制(突触放大)对神经元树突棘密度影响的文章进行了荟萃分析。我们的结果表明,在诱导突触缩放的实验方案后,棘密度持续降低,与干预类型无关。然后,我们讨论了我们的发现对当前关于稳态可塑性诱导的形态学变化的知识的意义。