The role of mitogen-activated protein kinase (MAPK) in morphine tolerance and dependence.
Journal Article (Journal Article;Review)
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.
Full Text
Duke Authors
Cited Authors
- Chen, Y; Sommer, C
Published Date
- October 2009
Published In
Volume / Issue
- 40 / 2
Start / End Page
- 101 - 107
PubMed ID
- 19468867
International Standard Serial Number (ISSN)
- 0893-7648
Digital Object Identifier (DOI)
- 10.1007/s12035-009-8074-z
Language
- eng
Conference Location
- United States