Todorova Vyara, Blokland Arjan
Institute II for Anatomy, Medical Faculty, University of Cologne, Cologne, Germany.
Curr Neuropharmacol. 2017;15(1):166-173. doi: 10.2174/1570159x14666160414111821.
Synaptic plasticity in the adult brain is believed to represent the cellular mechanisms of learning and memory. Mitochondria are involved in the regulation of the complex processes of synaptic plasticity. This paper reviews the current knowledge on the regulatory roles of mitochondria in the function and plasticity of synapses and the implications of mitochondrial dysfunctions in synaptic transmission. First, the importance of mitochondrial distribution and motility for maintenance and strengthening of dendritic spines, but also for new spines/synapses formation is presented. Secondly, the major mitochondrial functions as energy supplier and calcium buffer organelles are considered as possible explanation for their essential and regulatory roles in neuronal plasticity processes. Thirdly, the effects of synaptic potentiation on mitochondrial gene expression are discussed. And finally, the relation between age-related alterations in synaptic plasticity and mitochondrial dysfunctions is considered. It appears that memory loss and neurodegeneration during aging are related to mitochondrial (dys)function. Although, it is clear that mitochondria are essential for synaptic plasticity, further studies are indicated to scrutinize the intracellular and molecular processes that regulate the functions of mitochondria in synaptic plasticity.
成人大脑中的突触可塑性被认为代表了学习和记忆的细胞机制。线粒体参与突触可塑性复杂过程的调节。本文综述了目前关于线粒体在突触功能和可塑性中的调节作用的知识,以及线粒体功能障碍在突触传递中的影响。首先,介绍了线粒体分布和运动性对于维持和强化树突棘以及形成新的树突棘/突触的重要性。其次,线粒体作为能量供应者和钙缓冲细胞器的主要功能被视为其在神经元可塑性过程中发挥重要和调节作用的可能解释。第三,讨论了突触增强对线粒体基因表达的影响。最后,考虑了与年龄相关的突触可塑性改变和线粒体功能障碍之间的关系。衰老过程中的记忆丧失和神经退行性变似乎与线粒体(功能)异常有关。尽管线粒体对突触可塑性至关重要这一点很明确,但仍需进一步研究来仔细审查调节线粒体在突触可塑性中功能的细胞内和分子过程。