生物学杂志

生物学杂志 ›› 2025, Vol. 42 ›› Issue (1): 83-.doi: 10.3969/j.issn.2095-1736.2025.01.083

• 研究报告 • 上一篇    下一篇

多巴胺调控秀丽隐杆线虫遗忘的机制研究

朱　曼， 李若冰   

  1. 曲靖师范学院 生物资源与食品工程学院， 曲靖 655011
  • 出版日期:2025-02-18 发布日期:2025-02-12
  • 通讯作者: 朱曼，博士，讲师，主要从事以秀丽隐杆线虫为模型的学习、记忆、遗忘机制研究，E-mail:1506053001@qq.com
  • 作者简介:朱曼，博士，讲师，主要从事以秀丽隐杆线虫为模型的学习、记忆、遗忘机制研究，E-mail:1506053001@qq.com；李若冰，研究方向为遗忘分子机制研究，E-mail:1957912734@qq.com；朱曼和李若冰为共同第一作者
  • 基金资助:
    云南省科技厅基础研究专项青年项目（202301AU070215）

Study on the mechanism of dopamine regulating forgetting in Caenorhabditis elegans

ZHU Man, LI Ruobing   

  1. College of Biological Resource and Food Engineering, Qujing Normal University, Qujing 655011, China
  • Online:2025-02-18 Published:2025-02-12

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摘要： 为探究多巴胺信号途径在遗忘中的作用及分子调控机制，利用秀丽隐杆线虫食物－丁酮正向联想性学习模型对多巴胺信号途径关键组分进行筛选，包括酪氨酸羟化酶（CAT-2）、多巴胺转运体（DAT-1）、多巴胺受体（DOP-1/2/3/4）、G蛋白以及下游cAMP和PLC途径。结果显示：cat-2突变或6-OHDA处理阻碍了多巴胺信号的正常传递，从而导致线虫的学习和记忆保留能力明显下降；dat-1突变导致多巴胺的重摄取功能受阻，表现为加速遗忘；dop-1突变株的记忆保留存在缺陷，而dop-2、dop-3和dop-4突变株与对照组无明显差异；在筛选作用于多巴胺受体下游的G蛋白GSA-1、GOA-1、EGL-30中，仅gsa-1突变加速了遗忘。此外，对多巴胺下游的cAMP和PLC途径关键成员进行筛选，发现cAMP途径中kin-2（PKA）的突变加速遗忘发生。结果表明，在秀丽隐杆线虫中，多巴胺可能通过DOP-1/GSA-1/PKA通路参与调控遗忘。这些实验结果将为多巴胺在遗忘方面的研究提供理论依据，并为比较多巴胺系统在物种进化上的相似性和差异性提供参考。

关键词: 多巴胺, 秀丽隐杆线虫, 食物-丁酮正向联想性学习模型, 突变株, cAMP途径

Abstract: To investigate the role and molecular regulation mechanism of dopamine signaling pathway in forgetting, the key components of this pathway were screened using theCaenorhabditis elegansfood-butanone positive associative learning model, including tyrosine hydroxylase (CAT-2), dopamine transporter (DAT-1), dopamine receptor (DOP-1/2/3/4), G protein, cAMP and PLC pathways. The results showed that mutations incat-2or treatment with 6-OHDA disrupted normal dopamine signal transmission, leading to a notable decline in the worm’s learning and memory retention abilities. Mutations indat-1impeded dopamine reuptake, resulting in accelerated forgetting.dop-1mutant animals exhibited memory retention deficits, whiledop-2,dop-3, anddop-4mutants showed no significant difference from the control group. Among the screened G proteins (GSA-1, GOA-1, EGL-30), onlygsa-1mutation accelerated forgetting. Additionally, key members of the cAMP and PLC pathways were examined, revealing that mutations inkin-2(PKA) within the cAMP pathway expedited forgetting. The findings suggested that dopamine played a role in the regulation of forgetting inC. elegans, potentially acting through the DOP-1/GSA-1/PKA pathway. This study provided a theoretical foundation for understanding the role of dopamine in forgetting and offers insights into the comparison of dopamine systems across species evolution.

Key words: dopamine;Caenorhabditis elegans, the food-butanone positive association learning model, mutant, cAMP pathway

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