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Trends Pharmacol Sci. 2016 Feb;37(2):153-166. doi: 10.1016/j.tips.2015.11.001. Epub 2015 Dec 7.

CaM Kinases: From Memories to Addiction.

Author information

1
Department of Psychiatry and Psychotherapy, University Hospital, Friedrich-Alexander-University Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany; MRC Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, UK. Electronic address: Christian.Mueller@uk-erlangen.de.
2
Experimental and Clinical Pharmacopsychology, Psychiatric Hospital of the University of Zurich, Lenggstrasse 31, CH-8032 Zurich, Switzerland.
3
Division of Child Health, Obstetrics, and Gynaecology, School of Medicine, University of Nottingham, NG7 2UH, UK.
4
Department of Psychiatry and Psychotherapy, University Hospital, Friedrich-Alexander-University Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany.
5
MRC Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, UK.
6
Centre for the Cellular Basis of Behaviour, Institute of Psychiatry, King's College London, James Black Centre, 125 Coldharbour Lane, London SE5 8AF, UK.

Abstract

Drug addiction is a major psychiatric disorder with a neurobiological basis that is still insufficiently understood. Initially, non-addicted, controlled drug consumption and drug instrumentalization are established. They comprise highly systematic behaviours acquired by learning and the establishment of drug memories. Ca(2+)/calmodulin-dependent protein kinases (CaMKs) are important Ca(2+) sensors translating glutamatergic activation into synaptic plasticity during learning and memory formation. Here we review the role of CaMKs in the establishment of drug-related behaviours in animal models and in humans. Converging evidence now shows that CaMKs are a crucial mechanism of how addictive drugs induce synaptic plasticity and establish various types of drug memories. Thereby, CaMKs are not only molecular relays for glutamatergic activity but they also directly control dopaminergic and serotonergic activity in the mesolimbic reward system. They can now be considered as major molecular pathways translating normal memory formation into establishment of drug memories and possibly transition to drug addiction.

KEYWORDS:

Ca(2+)/calmodulin-dependent protein kinase; addiction; alcohol; drug dependence; opioids; psychostimulants

PMID:
26674562
DOI:
10.1016/j.tips.2015.11.001
[Indexed for MEDLINE]
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