1H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant mice

Respiratory depression is the leading cause of death in opioid overdose and is closely associated with the development of tolerance following repeated morphine use. However, the neurochemical adaptations in brainstem regions that regulate breathing, particularly under chronic opioid exposure, remain...

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Main Authors: Ozra Dehkordi, Stephen Lin, Safia Mohamud, Richard M. Millis, Paul C. Wang
Format: Article
Language:English
Published: Elsevier 2025-01-01
Series:Current Research in Physiology
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Online Access:http://www.sciencedirect.com/science/article/pii/S2665944125000094
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author Ozra Dehkordi
Stephen Lin
Safia Mohamud
Richard M. Millis
Paul C. Wang
author_facet Ozra Dehkordi
Stephen Lin
Safia Mohamud
Richard M. Millis
Paul C. Wang
author_sort Ozra Dehkordi
collection DOAJ
description Respiratory depression is the leading cause of death in opioid overdose and is closely associated with the development of tolerance following repeated morphine use. However, the neurochemical adaptations in brainstem regions that regulate breathing, particularly under chronic opioid exposure, remain poorly understood. G-protein-gated inwardly rectifying potassium (GIRK) channels, especially the GIRK2 subunit, are expressed in rhythm-generating neurons of the pre-Bötzinger complex and have been implicated in opioid-induced respiratory depression. Nonetheless, their specific role in morphine-induced neurochemical changes is not yet fully defined. In this study, in vivo proton magnetic resonance spectroscopy (1H MRS) was used in mice to assess morphine-induced metabolite changes in ventral brainstem regions encompassing the pre-Bötzinger complex. Wild-type mice were compared with GIRK2 heterozygous (GIRK2+/−) mutants. Baseline levels of several metabolites including glutamate (Glu), myo-inositol (Ins), N-acetylaspartate plus N-acetylaspartylglutamate (NAA + NAAG), and glutamate plus glutamine (Glu + Gln) differed significantly between GIRK2+/− and wild-type mice. Despite these baseline differences, many of morphine's effects on metabolite levels were similar in the wild-type and GIRK2+/− mice. Morphine increased phosphocreatine (PCr) in both genotypes, while total creatine (Cr + PCr) decreased only in the wild-type mice. Glutamine levels increased significantly in both groups. Notably, NAA decreased in wild-type but increased in GIRK2+/− mice, whereas NAA + NAAG decreased in both. These findings demonstrate that chronic morphine exposure induces substantial neurochemical changes in brainstem respiratory centers. Although the GIRK2+/ - mutation altered some of the metabolite responses, it does not fully block morphine's effects, highlighting the complexity of opioid-induced adaptations in the respiratory control networks.
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spelling doaj-art-78a1b5d9b2ee467493cf154b6dc24dcd2025-08-20T02:30:18ZengElsevierCurrent Research in Physiology2665-94412025-01-01810014710.1016/j.crphys.2025.1001471H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant miceOzra Dehkordi0Stephen Lin1Safia Mohamud2Richard M. Millis3Paul C. Wang4Department of Neurology, Howard University Hospital, Washington, D.C. 20060, United States; Corresponding author.Department of Radiology, Howard University Hospital, Washington, D.C. 20060, United StatesDepartment of Neurology, Howard University Hospital, Washington, D.C. 20060, United StatesDepartment of Physiology, American University of Antigua College of Medicine, Antigua and BarbudaDepartment of Radiology, Howard University Hospital, Washington, D.C. 20060, United States; Department of Physics, Fu Jen Catholic University, Taipei, TaiwanRespiratory depression is the leading cause of death in opioid overdose and is closely associated with the development of tolerance following repeated morphine use. However, the neurochemical adaptations in brainstem regions that regulate breathing, particularly under chronic opioid exposure, remain poorly understood. G-protein-gated inwardly rectifying potassium (GIRK) channels, especially the GIRK2 subunit, are expressed in rhythm-generating neurons of the pre-Bötzinger complex and have been implicated in opioid-induced respiratory depression. Nonetheless, their specific role in morphine-induced neurochemical changes is not yet fully defined. In this study, in vivo proton magnetic resonance spectroscopy (1H MRS) was used in mice to assess morphine-induced metabolite changes in ventral brainstem regions encompassing the pre-Bötzinger complex. Wild-type mice were compared with GIRK2 heterozygous (GIRK2+/−) mutants. Baseline levels of several metabolites including glutamate (Glu), myo-inositol (Ins), N-acetylaspartate plus N-acetylaspartylglutamate (NAA + NAAG), and glutamate plus glutamine (Glu + Gln) differed significantly between GIRK2+/− and wild-type mice. Despite these baseline differences, many of morphine's effects on metabolite levels were similar in the wild-type and GIRK2+/− mice. Morphine increased phosphocreatine (PCr) in both genotypes, while total creatine (Cr + PCr) decreased only in the wild-type mice. Glutamine levels increased significantly in both groups. Notably, NAA decreased in wild-type but increased in GIRK2+/− mice, whereas NAA + NAAG decreased in both. These findings demonstrate that chronic morphine exposure induces substantial neurochemical changes in brainstem respiratory centers. Although the GIRK2+/ - mutation altered some of the metabolite responses, it does not fully block morphine's effects, highlighting the complexity of opioid-induced adaptations in the respiratory control networks.http://www.sciencedirect.com/science/article/pii/S26659441250000941H MRSPre-bötzingerMorphineGIRK2 channels
spellingShingle Ozra Dehkordi
Stephen Lin
Safia Mohamud
Richard M. Millis
Paul C. Wang
1H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant mice
Current Research in Physiology
1H MRS
Pre-bötzinger
Morphine
GIRK2 channels
title 1H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant mice
title_full 1H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant mice
title_fullStr 1H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant mice
title_full_unstemmed 1H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant mice
title_short 1H MRS-based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild-type and GIRK2 mutant mice
title_sort 1h mrs based metabolite changes at ventral respiratory control centers of the medulla oblongata following administration of morphine in wild type and girk2 mutant mice
topic 1H MRS
Pre-bötzinger
Morphine
GIRK2 channels
url http://www.sciencedirect.com/science/article/pii/S2665944125000094
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