Rothwell Cailin M, de Hoog Eric, Spencer Gaynor E
Department of Biological Sciences, Brock University, St. Catharines, Ontario, Canada.
Department of Biological Sciences, Brock University, St. Catharines, Ontario, Canada
J Neurophysiol. 2017 Feb 1;117(2):692-704. doi: 10.1152/jn.00737.2016. Epub 2016 Nov 16.
Trophic factors can influence many aspects of nervous system function, such as neurite outgrowth, synapse formation, and synapse modulation. The vitamin A metabolite, retinoic acid, can exert trophic effects to promote neuronal survival and outgrowth in many species and is also known to modulate vertebrate hippocampal synapses. However, its role in synaptogenesis has not been well studied, and whether it can modulate existing invertebrate synapses is also not known. In this study, we first examined a potential trophic effect of retinoic acid on the formation of excitatory synapses, independently of its role in neurite outgrowth, using cultured neurons of the mollusc Lymnaea stagnalis We also investigated its role in modulating both chemical and electrical synapses between various Lymnaea neurons in cell culture. Although we found no evidence to suggest retinoic acid affected short-term synaptic plasticity in the form of post-tetanic potentiation, we did find a significant cell type-specific modulation of electrical synapses. Given the prevalence of electrical synapses in invertebrate nervous systems, these findings highlight the potential for retinoic acid to modulate network function in the central nervous system of at least some invertebrates.
NEW & NOTEWORTHY: This study performed the first electrophysiological analysis of the ability of the vitamin A metabolite, retinoic acid, to exert trophic influences during synaptogenesis independently of its effects in supporting neurite outgrowth. It was also the first study to examine the ability of retinoic acid to modify both chemical and electrical synapses in any invertebrate, nonchordate species. We provide evidence that all-trans retinoic acid can modify invertebrate electrical synapses of central neurons in a cell-specific manner.
营养因子可影响神经系统功能的许多方面,如神经突生长、突触形成和突触调制。维生素A代谢产物视黄酸可发挥营养作用,促进多种物种的神经元存活和生长,并且已知可调节脊椎动物的海马突触。然而,其在突触形成中的作用尚未得到充分研究,其是否能调节现有的无脊椎动物突触也不清楚。在本研究中,我们首先使用椎实螺的培养神经元,研究视黄酸对兴奋性突触形成的潜在营养作用,独立于其在神经突生长中的作用。我们还研究了其在调节细胞培养中各种椎实螺神经元之间的化学和电突触方面的作用。尽管我们没有发现证据表明视黄酸以强直后增强的形式影响短期突触可塑性,但我们确实发现了电突触存在显著的细胞类型特异性调制。鉴于电突触在无脊椎动物神经系统中的普遍性,这些发现突出了视黄酸调节至少一些无脊椎动物中枢神经系统网络功能的潜力。
本研究首次对视黄酸这种维生素A代谢产物在突触形成过程中发挥营养影响的能力进行了电生理分析,独立于其在支持神经突生长方面的作用。这也是首次研究视黄酸对任何无脊椎、非脊索动物物种的化学和电突触进行修饰的能力。我们提供的证据表明,全反式视黄酸可以以细胞特异性方式修饰中枢神经元的无脊椎动物电突触。