Huang Tzu-Ting, Matsuyama Hironori J, Tsukada Yuki, Singhvi Aakanksha, Syu Ru-Ting, Lu Yun, Shaham Shai, Mori Ikue, Pan Chun-Liang
Neuroscience Institute, Graduate School of Science, Nagoya University, Nagoya, Japan.
Group of Molecular Neurobiology, Graduate School of Science, Nagoya University, Nagoya, Japan.
Aging Cell. 2020 May;19(5):e13146. doi: 10.1111/acel.13146. Epub 2020 Apr 19.
Age-dependent cognitive and behavioral deterioration may arise from defects in different components of the nervous system, including those of neurons, synapses, glial cells, or a combination of them. We find that AFD, the primary thermosensory neuron of Caenorhabditis elegans, in aged animals is characterized by loss of sensory ending integrity, including reduced actin-based microvilli abundance and aggregation of thermosensory guanylyl cyclases. At the functional level, AFD neurons in aged animals are hypersensitive to high temperatures and show sustained sensory-evoked calcium dynamics, resulting in a prolonged operating range. At the behavioral level, senescent animals display cryophilic behaviors that remain plastic to acute temperature changes. Excessive cyclase activity of the AFD-specific guanylyl cyclase, GCY-8, is associated with developmental defects in AFD sensory ending and cryophilic behavior. Surprisingly, loss of the GCY-8 cyclase domain reduces these age-dependent morphological and behavioral changes, while a prolonged AFD operating range still exists in gcy-8 animals. The lack of apparent correlation between age-dependent changes in the morphology or stimuli-evoked response properties of primary sensory neurons and those in related behaviors highlights the importance of quantitative analyses of aging features when interpreting age-related changes at structural and functional levels. Our work identifies aging hallmarks in AFD receptive ending, temperature-evoked AFD responses, and experience-based thermotaxis behavior, which serve as a foundation to further elucidate the neural basis of cognitive aging.
年龄依赖性的认知和行为衰退可能源于神经系统不同组成部分的缺陷,包括神经元、突触、胶质细胞或它们的组合。我们发现,秀丽隐杆线虫的主要热感觉神经元AFD在老年动物中表现为感觉末梢完整性丧失,包括基于肌动蛋白的微绒毛丰度降低和热感觉鸟苷酸环化酶聚集。在功能水平上,老年动物中的AFD神经元对高温高度敏感,并表现出持续的感觉诱发钙动力学,导致作用范围延长。在行为水平上,衰老动物表现出嗜冷行为,对急性温度变化仍具有可塑性。AFD特异性鸟苷酸环化酶GCY-8的环化酶活性过高与AFD感觉末梢的发育缺陷和嗜冷行为有关。令人惊讶的是,GCY-8环化酶结构域的缺失减少了这些年龄依赖性的形态和行为变化,而在gcy-8动物中仍存在延长的AFD作用范围。初级感觉神经元的形态或刺激诱发反应特性的年龄依赖性变化与相关行为的变化之间缺乏明显相关性,这突出了在解释结构和功能水平上与年龄相关的变化时对衰老特征进行定量分析的重要性。我们的工作确定了AFD感受末梢、温度诱发的AFD反应和基于经验的趋温行为中的衰老标志,这为进一步阐明认知衰老的神经基础奠定了基础。