The role of mitogen-activated protein kinase (MAPK) in morphine tolerance and dependence.
Despite the existence of a large body of information on the subject, the mechanisms of morphine tolerance and dependence are not yet fully understood. There is substantial evidence indicating that mitogen-activated protein kinase (MAPK), a family including extracellular signal-regulated protein kinase, p38 MAPK, and c-Jun N-terminal kinase, can be activated by chronic morphine treatment in the central and peripheral nervous systems and that application of a MAPK inhibitor reduces morphine tolerance and dependence. While the exact mechanism is not completely understood, recent evidence suggests that the activation of MAPK induced by long-term morphine exposure may participate in tolerance and dependence by regulating the downstream targets, such as calcitonin gene-related peptide, substance P, nitric oxide, transient receptor potential vanilloid 1, and proinflammatory cytokines. In this review, we focus on the current understanding of the role of MAPK signaling pathways in morphine tolerance and dependence.
Duke Scholars
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Related Subject Headings
- Signal Transduction
- Neurology & Neurosurgery
- Morphine Dependence
- Mitogen-Activated Protein Kinases
- Humans
- Drug Tolerance
- Animals
- 3209 Neurosciences
- 3101 Biochemistry and cell biology
- 1702 Cognitive Sciences
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Signal Transduction
- Neurology & Neurosurgery
- Morphine Dependence
- Mitogen-Activated Protein Kinases
- Humans
- Drug Tolerance
- Animals
- 3209 Neurosciences
- 3101 Biochemistry and cell biology
- 1702 Cognitive Sciences