The Role of CaMKII and ERK Signaling in Addiction

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 Ca<sup>2+</sup>/calmodulin-dependent protein kinase...

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Main Authors: Wenbin Jia, Ichiro Kawahata, An Cheng, Kohji Fukunaga
Format: Article
Language:English
Published: MDPI AG 2021-03-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/22/6/3189
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author Wenbin Jia
Ichiro Kawahata
An Cheng
Kohji Fukunaga
author_facet Wenbin Jia
Ichiro Kawahata
An Cheng
Kohji Fukunaga
author_sort Wenbin Jia
collection DOAJ
description 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 Ca<sup>2+</sup>/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 psychostimulant-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.
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spelling doaj.art-d2e8ce3471624c4f902344c61e781dcc2023-11-21T11:21:32ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-03-01226318910.3390/ijms22063189The Role of CaMKII and ERK Signaling in AddictionWenbin Jia0Ichiro Kawahata1An Cheng2Kohji Fukunaga3Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, JapanDepartment of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, JapanDepartment of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, JapanDepartment of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, JapanNicotine 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 Ca<sup>2+</sup>/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 psychostimulant-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.https://www.mdpi.com/1422-0067/22/6/3189nicotine-induced addictionCa<sup>2+</sup>/calmodulin-dependent protein kinase IIextracellular signal-regulated kinasedopamine D1 receptordopamine D2 receptorfatty acid-binding protein 3
spellingShingle Wenbin Jia
Ichiro Kawahata
An Cheng
Kohji Fukunaga
The Role of CaMKII and ERK Signaling in Addiction
International Journal of Molecular Sciences
nicotine-induced addiction
Ca<sup>2+</sup>/calmodulin-dependent protein kinase II
extracellular signal-regulated kinase
dopamine D1 receptor
dopamine D2 receptor
fatty acid-binding protein 3
title The Role of CaMKII and ERK Signaling in Addiction
title_full The Role of CaMKII and ERK Signaling in Addiction
title_fullStr The Role of CaMKII and ERK Signaling in Addiction
title_full_unstemmed The Role of CaMKII and ERK Signaling in Addiction
title_short The Role of CaMKII and ERK Signaling in Addiction
title_sort role of camkii and erk signaling in addiction
topic nicotine-induced addiction
Ca<sup>2+</sup>/calmodulin-dependent protein kinase II
extracellular signal-regulated kinase
dopamine D1 receptor
dopamine D2 receptor
fatty acid-binding protein 3
url https://www.mdpi.com/1422-0067/22/6/3189
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