Regulation of extinction of cocaine-induced place preference by midkine is related to a differential phosphorylation of peroxiredoxin 6 in dorsal striatum

Gramage, Esther; Pérez-Garcı́a, Carmen; Vicente-Rodríguez, Marta; Bollen, Silke; Rojo, Loreto; Herradón, Gonzalo

doi:10.1016/j.bbr.2013.07.026

Cited by 21 publications

(35 citation statements)

References 47 publications

(71 reference statements)

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“…Mdk −/− mice are more sensitive to the anxiolytic effects of diazepam (Vicente-Rodriguez et al , 2014) and show reduced extinction to cocaine conditioned place preference (Gramage et al , 2013). Mdk expression is also induced in the VTA, the nucleus accumbens, and the hippocampus in response to morphine administration (Ezquerra et al , 2007, Garcia-Perez et al , 2015, Garcia-Perez et al , 2014).…”

Section: Discussionmentioning

confidence: 99%

Midkine in the mouse ventral tegmental area limits ethanol intake and Ccl2 gene expression

Lasek

2017

Genes Brain and Behavior

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Midkine (MDK) is a cytokine and neurotrophic factor that is more highly expressed in the brains of human alcoholics and in mice predisposed to drink large amounts of ethanol, suggesting that MDK may regulate ethanol consumption. Here we measured ethanol consumption in male and female Mdk knockout (−/−) mice using the two-bottle choice and the drinking in the dark (DID) tests. We found that Mdk −/− mice consumed significantly more ethanol than wild type controls in both tests. To determine if MDK acts in the ventral tegmental area (VTA) to regulate ethanol consumption, we delivered lentivirus expressing a Mdk shRNA into the VTA of male C57BL/6J mice to locally knockdown Mdk and performed the DID test. Mice expressing a Mdk shRNA in the VTA consumed more ethanol than mice expressing a control non-targeting shRNA, demonstrating that the VTA is one site in the brain through which MDK acts to regulate ethanol consumption. Since MDK also controls the expression of inflammatory cytokines in other organs, we examined gene expression of interleukin-1 beta (Il1b), tumor necrosis factor alpha (Tnf) and the chemokine (C-C motif) ligand 2 (Ccl2) in the VTA of Mdk −/− mice and in mice expressing Mdk shRNA in the VTA. Expression of Ccl2 was elevated in the VTA of Mdk −/− mice and in mice expressing Mdk shRNA in the VTA. These results demonstrate that MDK functions in the VTA to limit ethanol consumption and levels of CCL2, a chemokine known to increase ethanol consumption.

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Section: Discussionmentioning

confidence: 99%

Midkine in the mouse ventral tegmental area limits ethanol intake and Ccl2 gene expression

Lasek

2017

Genes Brain and Behavior

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“…However, in those studies it was shown that PTN‐/‐ mice maintain amphetamine‐induced CPP 5 days after the last injection of amphetamine whereas WT+/+ and MK‐/‐ mice did not maintain amphetamine‐induced CPP (Gramage et al ., ; Martín et al ., ), suggesting a role for endogenous PTN in the loss of amphetamine‐induced CPP. In contrast, we recently found that genetic deletion of MK strikingly decreases the capacity of mice to eradicate cocaine‐induced CPP (Gramage et al ., 2013b). The data support the notion that the absence of endogenous PTN or MK is a risk factor for amphetamine or cocaine relapse, respectively, after drug withdrawal and suggest that mutations on the PTN/MK genes leading to a loss of their functions or low levels of their expression in humans could underlie an individual increased vulnerability to amphetamine and cocaine relapse.…”

Section: Roles Of Mk and Ptn In Addiction And Neurodegenerationmentioning

confidence: 99%

Targeting midkine and pleiotrophin signalling pathways in addiction and neurodegenerative disorders: recent progress and perspectives

Herradón

Pérez-Garcı́a

2014

British J Pharmacology

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Midkine (MK) and pleiotrophin (PTN) are two neurotrophic factors that are highly up-regulated in different brain regions after the administration of various drugs of abuse and in degenerative areas of the brain. A deficiency in both MK and PTN has been suggested to be an important genetic factor, which confers vulnerability to the development of the neurodegenerative disorders associated with drugs of abuse in humans. In this review, evidence demonstrating that MK and PTN limit the rewarding effects of drugs of abuse and, potentially, prevent drug relapse is compiled. There is also convincing evidence that MK and PTN have neuroprotective effects against the neurotoxicity and development of neurodegenerative disorders induced by drugs of abuse. Exogenous administration of MK and/or PTN into the CNS by means of non-invasive methods is proposed as a novel therapeutic strategy for addictive and neurodegenerative diseases. Identification of new molecular targets downstream of the MK and PTN signalling pathways or pharmacological modulation of those already known may also provide a more traditional, but probably effective, therapeutic strategy for treating addictive and neurodegenerative disorders. LINKED ARTICLESThis article is part of a themed section on Midkine. To view the other articles in this section visit http://dx.doi. org/10.1111/bph.2014.171.issue-4 Abbreviations ALDH1A1, aldehyde dehydrogenase family 1 member A1; ALK, anaplastic lymphoma kinase; ANXA7, annexin; BBB, blood brain barrier; CKMT1, creatine kinase U-type; COPS5, COP9 signalosome subunit 5; CPP, conditioned place preference; KA, kainic acid; MK, midkine; NGF, nerve growth factor; PD, Parkinson's disease; PTK, protein tyrosine kinase; PTN, pleiotrophin; PTP, protein tyrosine phosphatase; PTPRZ, protein tyrosine phosphatase type Z IntroductionThe neurotoxic effects of drugs of abuse underlie not only drug-seeking behaviours but also the neurodegeneration processes associated with chronic drug consumption . For example, chronic alcohol consumption is associated with an increase in the incidence of a variety of diseases, including CNS degeneration (Collins and Neafsey, 2012). These addictive and neurotoxic effects of psychostimulants and other drugs of abuse have been associated with enhanced damage of dopaminergic neurons in the nigrostriatal pathway (Ferrucci et al., 2008;Valverde and Rodríguez-Árias, 2013). Drugs of abuse promote the intracellular accumulation of dopamine (Kalivas and O'Brien, 2008), which could elicit neuronal death by blocking mitochondrial complex 1, as occurs, for example, with Parkinsonian agents (Fahn and Sulzer, 2004). In addition, cocaine has been shown to cause significant increases in α-synuclein levels in dopaminergic neurons (Mash et al., 2003). Interestingly, α-synuclein is known to be the main component of Lewy bodies in patients with Parkinson's disease (PD) (Spillantini et al., 1997). Furthermore, it was recently found that BJP British Journal of Pharmacology DOI:10.1111/bph.12312 www.brjpharmacol.org Briti...

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“…In a proteomic study similar to ours, the ACO2 activator fumarate hydratase was one of the few proteins whose expression in the NAcc of rats that extinguish cocaine-induced CPP differed from that in the NAcc of rats that do not [7]. Indeed, it has been shown that a greater magnitude of CPP extinction correlates with increased tyrosine phosphorylation of ACO2 in the mouse prefrontal cortex [13], whereas lower levels of phosphorylation in the prefrontal cortex were evident after extinction of morphine-induced CPP [40]. From these data, it could be suggested that the activation of ACO2 might be a useful biomarker for persistent cocaine or morphine use, as also supported by the differential regulation of this protein in the NAcc of LEW and F344 rats.…”

Section: This May Be Due To the Fact That Translation Can Be Tightly mentioning

confidence: 75%

“…PRDX6 belongs to the group of peroxiredoxin proteins, a ubiquitous family of antioxidant enzymes that control hydrogen peroxide levels and that regulate signal transduction in mammalian cells [27]. This protein seems to regulate some addiction-related phenomena and it has been shown that extinction of cocaine-induced conditioned place preference (CPP) by the growth factor midkine is correlated to the differential phosphorylation of PRDX6 in the dorsal striatum [13]. Interestingly, another member of the peroxiredoxin family, peroxiredoxin 2, was seen to be differentially regulated in the NAcc in response to a cocaine challenge when animals that do not extinguish cocaineinduced CPP were compared with those that do extinguish this behavior [7].…”

Section: This May Be Due To the Fact That Translation Can Be Tightly mentioning

confidence: 99%

Differential Protein Expression in the Nucleus Accumbens and Amygdala of Lewis and Fischer 344 Rats, and its Relevance in Drug Addiction

Roura-Martínez¹,

Ucha²,

Coria³

et al. 2014

Journal of Drug and Alcohol Research

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The Lewis (LEW) and Fischer 344 (F344) rat strains are widely used as models of genetic vulnerability to drug addiction, particularly since these two strains show different patterns of drug selfadministration. We previously performed an unbiased and genomewide microarray analysis to define the differences in gene expression in the nucleus accumbens (NAcc) and prefrontal cortex between LEW and F344 rats. In this study, we set out to determine the strain differences in the NAcc and amygdala at the protein level using bidimensional gel electrophoresis. As such, 11 proteins were found to be differentially expressed between these two strains, the activity of which was mainly related to vesicular trafficking (STXBP1 and GDI1), energy metabolism (ATP5B, ENO2, and ACOT7), and cytoskeletal formation. This information might be useful to search for new molecular targets to screen individuals at high risk of developing an addictive disorder.

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Regulation of extinction of cocaine-induced place preference by midkine is related to a differential phosphorylation of peroxiredoxin 6 in dorsal striatum

Cited by 21 publications

References 47 publications

Midkine in the mouse ventral tegmental area limits ethanol intake and Ccl2 gene expression

Midkine in the mouse ventral tegmental area limits ethanol intake and Ccl2 gene expression

Targeting midkine and pleiotrophin signalling pathways in addiction and neurodegenerative disorders: recent progress and perspectives

Differential Protein Expression in the Nucleus Accumbens and Amygdala of Lewis and Fischer 344 Rats, and its Relevance in Drug Addiction

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