The role of mitogen-activated protein kinase (MAPK) in morphine tolerance and dependence.

Published

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

Pubmed Central 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