{"title":"MiR-33-5p 调节 CREB 以诱导大鼠的吗啡状态依赖记忆:与μ阿片受体的相互作用。","authors":"Sadegh Moradi Vastegani, Behrang Alani, Khatereh Kharazmi, Abolfazl Ardjmand","doi":"10.22088/IJMCM.BUMS.11.2.150","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":14152,"journal":{"name":"International Journal of Molecular and Cellular Medicine","volume":null,"pages":null},"PeriodicalIF":1.5000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/91/43/ijmcm-11-150.PMC10116354.pdf","citationCount":"0","resultStr":"{\"title\":\"MiR-33-5p Regulates CREB to Induce Morphine State-dependent Memory in Rats: Interaction with the µ Opioid Receptor.\",\"authors\":\"Sadegh Moradi Vastegani, Behrang Alani, Khatereh Kharazmi, Abolfazl Ardjmand\",\"doi\":\"10.22088/IJMCM.BUMS.11.2.150\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":14152,\"journal\":{\"name\":\"International Journal of Molecular and Cellular Medicine\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2022-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/91/43/ijmcm-11-150.PMC10116354.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Molecular and Cellular Medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.22088/IJMCM.BUMS.11.2.150\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/2/1 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Molecular and Cellular Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22088/IJMCM.BUMS.11.2.150","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/2/1 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
MiR-33-5p Regulates CREB to Induce Morphine State-dependent Memory in Rats: Interaction with the µ Opioid Receptor.
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.
期刊介绍:
The International Journal of Molecular and Cellular Medicine (IJMCM) is a peer-reviewed, quarterly publication of Cellular and Molecular Biology Research Center (CMBRC), Babol University of Medical Sciences, Babol, Iran. The journal covers all cellular & molecular biology and medicine disciplines such as the genetic basis of disease, biomarker discovery in diagnosis and treatment, genomics and proteomics, bioinformatics, computer applications in human biology, stem cells and tissue engineering, medical biotechnology, nanomedicine, cellular processes related to growth, death and survival, clinical biochemistry, molecular & cellular immunology, molecular and cellular aspects of infectious disease and cancer research. IJMCM is a free access journal. All open access articles published in IJMCM are distributed under the terms of the Creative Commons Attribution CC BY. The journal doesn''t have any submission and article processing charges (APCs).