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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MDPI AG
2021-03-01
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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. |
first_indexed | 2024-03-10T13:03:17Z |
format | Article |
id | doaj.art-d2e8ce3471624c4f902344c61e781dcc |
institution | Directory Open Access Journal |
issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-10T13:03:17Z |
publishDate | 2021-03-01 |
publisher | MDPI AG |
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series | International Journal of Molecular Sciences |
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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