Journal
NEUROPHARMACOLOGY
Volume 56, Issue -, Pages 73-82Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuropharm.2008.06.059
Keywords
Growth factors; Drug addiction; Dendritic spines; Brain derived neurotrophic factor; Nerve growth factor; Intracellular signaling; Neurotrophic factors; Morphine; Cocaine; Reward; Relapse; Actin polymerization; Neuron Morphology; ERK; Akt; PI3 kinase; NF kappa B; LTD; LTP
Categories
Funding
- NIDA NIH HHS [R01 DA014133, R01 DA014133-08, R01 DA014133-09] Funding Source: Medline
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA014133] Funding Source: NIH RePORTER
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Drugs of abuse produce widespread effects on the Structure and function of neurons throughout the brain's reward circuitry, and these changes are believed to underlie the long-lasting behavioral phenotypes that characterize addiction. Although the intracellular mechanisms regulating the structural plasticity of neurons are not fully understood, accumulating evidence suggests all essential role for neurotrophic factor signaling in the neuronal remodeling which Occurs after chronic drug administration. Brain-derived neurotrophic factor (BDNF), a growth factor enriched in brain and highly regulated by several drugs of abuse, regulates the phosphatidylinositol 3'-kinase (PI3K), mitogen-activated protein kinase (MAPK), phospholipase C gamma (PLC gamma), and nuclear factor kappa B (NF kappa B) signaling pathways, which influence a range of cellular functions including neuronal survival, growth, differentiation, and structure. This review discusses recent advances in our understanding of how BDNF and its signaling pathways regulate structural and behavioral plasticity in the context of drug addiction. (c) 2008 Elsevier Ltd. All rights reserved.
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