The role of CamkII and ERK signaling in addiction

Wenbin Jia, Ichiro Kawahata, An Cheng, Kohji Fukunaga

Research output: Contribution to journalReview articlepeer-review

2 Citations (Scopus)

Abstract

Nicotine is the predominant addictive compound of tobacco and causes the acquisition of dependence through its interactions with nicotinic acetylcholine receptors and various neurotransmitter releases in the central nervous system. The Ca2+/calmodulin-dependent protein kinase II (CaMKII) and extracellular signal-regulated kinase (ERK) play a pivotal role in synaptic plasticity in the hippocampus. CaMKII is involved in long-term potentiation induction, which underlies the consolidation of learning and memory; however, the roles of CaMKII in nicotine and other psy-chostimulant-induced addiction still require further investigation. This article reviews the molecular mechanisms and crucial roles of CaMKII and ERK in nicotine and other stimulant drug-induced addiction. We also discuss dopamine (DA) receptor signaling involved in nicotine-induced addiction in the brain reward circuitry. In the last section, we introduce the association of polyunsaturated fatty acids and cellular chaperones of fatty acid-binding protein 3 in the context of nicotine-induced addiction in the mouse nucleus accumbens and provide a novel target for the treatment of drug abuse affecting dopaminergic systems.

Original languageEnglish
Article number3189
Pages (from-to)1-19
Number of pages19
JournalInternational journal of molecular sciences
Volume22
Issue number6
DOIs
Publication statusPublished - 2021 Mar 2

Keywords

  • Ca/calmodulin-dependent protein kinase II
  • Dopamine D1 receptor
  • Dopamine D2 receptor
  • Extracellular signal-regulated kinase
  • Fatty acid-binding protein 3
  • Nicotine-induced addiction

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

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