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微小RNA-33-5p通过调控CREB诱导大鼠吗啡状态依赖性记忆:与μ阿片受体的相互作用

MiR-33-5p Regulates CREB to Induce Morphine State-dependent Memory in Rats: Interaction with the µ Opioid Receptor.

作者信息

Moradi Vastegani Sadegh, Alani Behrang, Kharazmi Khatereh, Ardjmand Abolfazl

机构信息

Institute for Basic Sciences, Physiology Research Center, Kashan University of Medical Sciences, Kashan, Iran.

Department of Applied Cell Sciences, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran.

出版信息

Int J Mol Cell Med. 2022;11(2):150-167. doi: 10.22088/IJMCM.BUMS.11.2.150. Epub 2023 Feb 1.

Abstract

The aim of the present study was to examine the hypothesis that miR-33-5p attenuates morphine state-dependent (StD) memory via the µ opioid receptor by regulating cyclic AMP response element-binding protein (CREB). The effects of post-training morphine and morphine StD memory and their interaction with pre-test naloxone were evaluated using a single-trial inhibitory avoidance paradigm. Then, the hippocampal miR-33-5p gene and pCREB/CREB protein expression profiles were evaluated using quantitative real-time PCR and western blotting, respectively. We found that while post-training morphine and morphine StD memory respectively up- and down-regulate the miR-33-5p expression profile in the hippocampus, the reverse results are true for the expression of pCREB/CREB. Pre-test naloxone antagonized the response. Overall, our findings suggest that the expression levels of miR-33-5p in the hippocampus set the basis for morphine StD memory with low miR-33-5p enabling state dependency. The mechanism is mediated via miR33-5p and CREB signaling with the interaction of the µ opioid receptor. This finding may be used as a potential strategy for ameliorating morphine-induced memory-related disorders.

摘要

本研究的目的是检验以下假设

即miR-33-5p通过调节环磷酸腺苷反应元件结合蛋白(CREB),经由μ阿片受体减弱吗啡状态依赖性(StD)记忆。使用单次试验抑制性回避范式评估训练后吗啡和吗啡StD记忆的作用及其与测试前纳洛酮的相互作用。然后,分别使用定量实时PCR和蛋白质免疫印迹法评估海马体中miR-33-5p基因和磷酸化CREB/ CREB蛋白的表达谱。我们发现,训练后吗啡和吗啡StD记忆分别上调和下调海马体中的miR-33-5p表达谱,而磷酸化CREB/CREB的表达则相反。测试前使用纳洛酮可拮抗该反应。总体而言,我们的研究结果表明,海马体中miR-33-5p的表达水平为吗啡StD记忆奠定了基础,低水平的miR-33-5p可实现状态依赖性。其机制是通过miR33-5p和CREB信号传导以及μ阿片受体的相互作用介导的。这一发现可能作为改善吗啡诱导的记忆相关障碍的潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c40d/10116354/7cb4210deec0/ijmcm-11-150-g001.jpg

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