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Role of hypothalamic-pituitary axis in morphine-induced alteration in thymic cell distribution using mu-opioid
S Roy1, J H Wang, S Balasubramanian
1Department of Pharmacology and Surgery, University of Minnesota and Veterans Administration Medical Center, 1 Veterans Drive, 55417, Minneapolis, MN, USA. royxx002@gold.tc.umn.edu
Abstract:
Mu-opioid receptor knockout mice (MORKO), were used to address two questions: (1) if morphine induced decrease in thymic weight and cell distribution is mediated by the mu-opioid receptor and (2) the role of corticosteroids in morphine mediated alteration in thymic cell distribution. Our result show that morphine mediated increase in plasma corticosterone is mediated by the mu-opioid receptor since morphine at doses as high as 25 mg/kg-body weight does not increase plasma corticosterone levels in the MORKO. In addition, we have also shown that morphine treatment results in the differentiation of CD4+CD8+ (double positive cells) to single positive CD4+ cells while dexamethasone treatment results in the deletion of CD4+CD8+ (double positive) cells.
Insights
Morphine
Area of Science:
- Immunology and Pharmacology
Background:
- The thymus is a primary lymphoid organ crucial for T-cell maturation.
- Opioid receptors, particularly the mu-opioid receptor, are known to influence immune function.
- Corticosteroids play a significant role in immune regulation and thymic function.
Purpose of the Study:
- To investigate if mu-opioid receptor (MOR) mediates morphine's effects on thymic weight and cell distribution.
- To determine the role of corticosteroids in morphine-induced alterations of thymic cell distribution.
Main Methods:
- Utilizing mu-opioid receptor knockout mice (MORKO) to assess morphine's effects in the absence of MOR.
- Administering morphine and dexamethasone to mice and analyzing plasma corticosterone levels.
- Evaluating thymic cell distribution using flow cytometry, focusing on CD4+CD8+ double-positive cells.
Main Results:
- Morphine-induced increase in plasma corticosterone is mediated by the mu-opioid receptor, as MORKO mice showed no increase.
- Morphine treatment led to the differentiation of CD4+CD8+ thymocytes into CD4+ single-positive cells.
- Dexamethasone treatment resulted in the deletion of CD4+CD8+ thymocytes.
Conclusions:
- The mu-opioid receptor is essential for mediating morphine's effects on corticosterone levels.
- Morphine and corticosteroids differentially affect thymic cell populations, suggesting distinct mechanisms of action.
- These findings highlight the complex interplay between opioid signaling, the hypothalamic-pituitary-adrenal axis, and thymic immune cell development.