Evidence for a role of CaMKIV in the development of opioid analgesic tolerance

Ko, Shanelle W.; Jia, Yongheng; Xu, Hui; Yim, Se Jeong; Jang, Dong Hyuk; Lee, Yong Seok; Zhao, Ming; Toyoda, Hiroki; Chatila, Talal A.; Kaang, Bong Kiun; Zhuo, Min

doi:10.1111/j.1460-9568.2006.04748.x

Cited by 22 publications

(21 citation statements)

References 62 publications

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“…wet-dog shakes, paw tremors, or jumping. There is no difference in these withdrawal signs between CaMKIV KO and WT mice, which suggests no role for CaMKIV in morphine withdrawal behaviors [107].…”

Section: Cppmentioning

confidence: 94%

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CaM Kinases: From Memories to Addiction

Müller

Quednow

Lourdusamy

et al. 2016

Trends in Pharmacological Sciences

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Drug addiction is a major psychiatric disorder with a neurobiological base 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 drugrelated behaviours in animal models and in humans. Converging evidence shows now 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; 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, drug dependence, addiction, psychostimulants, alcohol, opioids 3 Drug Use and AddictionDrug addiction is a major psychiatric disorder for which only limited therapies are currently available [1,2]. A striking criterion for drug abuse and addiction is that it severely threatens one's own and others well-being and health. As such, there is a persistent need to treat drug addiction effectively, and ideally reverse the behavioural repertoire of an affected individual back to normal.An important feature of drug addiction is that it develops from a behavioural repertoire, which is considered to be normal in many societies of the world: the controlled consumption and instrumentalization of psychoactive drugs [3,4].Establishing and maintaining controlled drug consumption is based on systematic learning and memory retrieval of distinct behaviours, related to drug seeking, preparation, and consumption in a specific context [5,6]. Thereby, information is encoded within different behavioural systems, which can be summarized as "drug memories" [5,[7][8][9] (Box 1). It is believed that an intensification of these memories together with a loss of impulse control (compulsivity) is responsible for the transition from controlled drug use to addiction [10][11][12]. Understanding how these drug memories are established and how they may take control over a normal behavioural repertoire should, therefore, allow to improve the prevention of addiction and to develop new and more effective treatments [13]. From Memories to Drug MemoriesIt was suggested that anatomical pathways, micro-morphological adaptations, as well as molecular mechanisms in the brain, overlap between normal learning and memory and drug memories [14][15][16]. A crucial player for memory formation in the brain is the glutamatergic system and its plasticity based on experience [17]. Addiction research considered glu...

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Section: Cppmentioning

confidence: 94%

“…This effect is most evident in the late phase of CPP consolidation 12h post conditioning [106]. CaMKIV is required for the establishment of morphine-induced CPP in mice, since CaMKIV KO mice show a significantly reduced CPP for morphine [107]. wet-dog shakes, paw tremors, or jumping.…”

Section: Cppmentioning

confidence: 99%

CaM Kinases: From Memories to Addiction

Müller

Quednow

Lourdusamy

et al. 2016

Trends in Pharmacological Sciences

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“…For example, when excess Ca ++ ions are present, neuronal toxicity occurs leading to neuron death or contributing to neurodegenerative diseases [204,206]. Inhibition of CaMK IV also leads to neuron death in cell cultures [207], and CaMK IV deficiency in mice results in loss of learning or memory or in less drug tolerance [208][209][210][211]. The ion channels involved in Ca ++ toxicity including the AMPA and NMDA receptors undergo alternative splicing [202,204], and inclusion of the NMDAR1 exons 5 and 21 is controlled by membrane depolarization and CaMK IV [84,104,105,107,212].…”

Section: Neuronal Death and Neurodegenerative Diseasesmentioning

confidence: 99%

Control of alternative pre-mRNA splicing by Ca++ signals

Xie¹

2008

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

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Alternative pre-mRNA splicing is a common way of gene expression regulation in metazoans. The selective use of specific exons can be modulated in response to various manipulations that alter Ca ++ signals, particularly in neurons. A number of splicing factors have also been found to be controlled by Ca ++ signals. Moreover, pre-mRNA elements have been identified that are essential and sufficient to mediate Ca ++ -regulated splicing, providing model systems for dissecting the involved molecular components. In neurons, this regulation likely contributes to the fine-tuning of neuronal properties.

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“…This mechanism contributes to opioid tolerance, because coadministration of NMDA inhibitor reduced analgesic tolerance to morphine (Elliot et al 1994). CaMK IV knock-out mice developed less analgesic tolerance than wild-type mice after chronic morphine treatment with no alteration in physical dependence or acute morphine-induced analgesia (Ko et al 2006). Furthermore, the increased phosphorylation of CREB observed in wild-type mice after chronic morphine treatment was absent in CaMK IV knock-out mice, indicating the role of CaMK IV in the development of opioid analgesic tolerance but not physical dependence (Ko et al 2006).…”

Section: Protein Phosphorylation/dephosphorylation In Opioid Tolerancmentioning

confidence: 97%

“…CaMK IV knock-out mice developed less analgesic tolerance than wild-type mice after chronic morphine treatment with no alteration in physical dependence or acute morphine-induced analgesia (Ko et al 2006). Furthermore, the increased phosphorylation of CREB observed in wild-type mice after chronic morphine treatment was absent in CaMK IV knock-out mice, indicating the role of CaMK IV in the development of opioid analgesic tolerance but not physical dependence (Ko et al 2006). Pretreatment or therapeutic treatment with PKA, PKC, or CaMK II inhibitors all could reverse morphine-induced analgesia tolerance in mice (Javed et al 2004;Smith et al 2007;Gabra et al 2008;Wang et al 2003).…”

Section: Protein Phosphorylation/dephosphorylation In Opioid Tolerancmentioning

confidence: 97%

Opioid Receptor Trafficking and Signaling: What Happens After Opioid Receptor Activation?

Bian

Wu²,

Su³

et al. 2011

Cell Mol Neurobiol

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Prolonged opioid treatment leads to a comprehensive cellular adaptation mediated by opioid receptors, a basis to understand the development of opioid tolerance and dependence. However, the molecular mechanisms underlying opioid-induced cellular adaptation remain obscure. Recent advances in opioid receptor trafficking and signaling in cells have extensively increased our insight into the network of intracellular signal integration. This review focuses on those important intracellular biochemical processes that play critical roles in the development of opioid tolerance and dependence after opioid receptor activation, and tries to explain what happens after opioid receptor activation, and how the cellular adaptation develops from cell membrane to nucleus. Decades of research have delineated a network on opioid receptor trafficking and signaling, but the challenge remains to explain opioid tolerance and dependence from a single cellular signal network.

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Evidence for a role of CaMKIV in the development of opioid analgesic tolerance

Cited by 22 publications

References 62 publications

CaM Kinases: From Memories to Addiction

CaM Kinases: From Memories to Addiction

Control of alternative pre-mRNA splicing by Ca++ signals

Opioid Receptor Trafficking and Signaling: What Happens After Opioid Receptor Activation?

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