Cifelli Jessica L, Dozier Lara, Chung Tim S, Patrick Gentry N, Yang Jerry
From the Department of Chemistry and Biochemistry and.
the Section of Neurobiology in the Division of Biological Sciences, University of California, San Diego, La Jolla, California 92093-0358.
J Biol Chem. 2016 Jun 3;291(23):11981-92. doi: 10.1074/jbc.M115.701482. Epub 2016 Mar 28.
The majority of excitatory synapses in the brain exist on dendritic spines. Accordingly, the regulation of dendritic spine density in the hippocampus is thought to play a central role in learning and memory. The development of novel methods to control spine density could, therefore, have important implications for treatment of a host of neurodegenerative and developmental cognitive disorders. Herein, we report the design and evaluation of a new class of benzothiazole amphiphiles that exhibit a dose-dependent response leading to an increase in dendritic spine density in primary hippocampal neurons. Cell exposure studies reveal that the increase in spine density can persist for days in the presence of these compounds, but returns to normal spine density levels within 24 h when the compounds are removed, demonstrating the capability to reversibly control spinogenic activity. Time-lapse imaging of dissociated hippocampal neuronal cultures shows that these compounds promote a net increase in spine density through the formation of new spines. Biochemical studies support that promotion of spine formation by these compounds is accompanied by Ras activation. These spinogenic molecules were also capable of inhibiting a suspected mechanism for dendritic spine loss induced by Alzheimer-related aggregated amyloid-β peptides in primary neurons. Evaluation of this new group of spinogenic agents reveals that they also exhibit relatively low toxicity at concentrations displaying activity. Collectively, these results suggest that small molecules that promote spine formation could be potentially useful for ameliorating cognitive deficiencies associated with spine loss in neurodegenerative diseases such as Alzheimer disease, and may also find use as general cognitive enhancers.
大脑中大多数兴奋性突触存在于树突棘上。因此,海马体中树突棘密度的调节被认为在学习和记忆中起着核心作用。因此,开发控制树突棘密度的新方法可能对治疗一系列神经退行性和发育性认知障碍具有重要意义。在此,我们报告了一类新型苯并噻唑两亲物的设计和评估,它们表现出剂量依赖性反应,导致原代海马神经元的树突棘密度增加。细胞暴露研究表明,在这些化合物存在的情况下,树突棘密度的增加可以持续数天,但当化合物被去除后,在24小时内会恢复到正常的树突棘密度水平,这表明其具有可逆控制树突棘生成活性的能力。解离的海马神经元培养物的延时成像显示,这些化合物通过形成新的树突棘促进树突棘密度的净增加。生化研究支持这些化合物促进树突棘形成的同时伴有Ras激活。这些树突棘生成分子还能够抑制原代神经元中由阿尔茨海默病相关的聚集淀粉样β肽诱导的树突棘丢失的一种推测机制。对这组新的树突棘生成剂的评估表明,它们在显示活性的浓度下也表现出相对较低的毒性。总的来说,这些结果表明,促进树突棘形成的小分子可能对改善与神经退行性疾病(如阿尔茨海默病)中树突棘丢失相关的认知缺陷具有潜在的用途,并且也可能用作一般的认知增强剂。