Functional neuroimaging of amphetamine-induced striatal neurotoxicity in the pleiotrophin knockout mouse model

Soto-Montenegro, María Luisa; Vicente-Rodríguez, Marta; Pérez-Garcı́a, Carmen; Gramage, Esther; Desco, Manuel; Herradón, Gonzalo

doi:10.1016/j.neulet.2015.02.041

Cited by 7 publications

(5 citation statements)

References 38 publications

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“…1C). Previously, rhTM has been reported to exert its anticoagulant and anti-inflammatory activity at a dose of 1-200 mg/kg (32)(33)(34)(35). In preliminary experiments, we evaluated the effects of rhTM on APAP-induced liver injury at a dose of 10 mg/ml, however, rhTM in this dose did not show significant suppression of liver damages (data not shown).…”

Section: Resultsmentioning

confidence: 91%

“…The mice in control and TM groups were sacrificed at 0, 2, 4, 24 and 48 h (n=10 at each time point/group) in this study. All amimals were euthanized by sevoflurane at concentrations of 4-5% for induction and 2-3% for maintenance, as described previously (35,36). The depth of anesthesia was confirmed by loss of the postural reaction and righting reflex (the pedal withdrawal reflex in the forelimbs and hind limbs, the tail pinch reflex, and the eyelid reflex).…”

Section: Methodsmentioning

confidence: 99%

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Recombinant human soluble thrombomodulin ameliorates acetaminophen‑induced liver toxicity in mice

et al. 2019

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Recombinant human soluble thrombomodulin alpha (rhTM) has been developed as an anticoagulant with anti-inflammatory activity. Notably, acetaminophen (APAP)-induced liver disease (AILI) is caused by direct metabolite-induced hepatotoxicity as well as hepatic hyper-coagulation. To evaluate the utility of anticoagulant for the treatment of AILI, rhTM was administered in a mouse AILI model and liver damage was analyzed. AILI was induced in 8-week-old mice by intraperitoneal injection of APAP. rhTM (20 mg/kg) or placebo was injected at the same time as APAP administration. Serum alanine aminotransferase, fibrin degradation products and high-mobility group box 1 levels were significantly decreased in the rhTM-treated group compared with the control group. Furthermore, rhTM reduced the necrotic area and fibrin deposition in liver sections. rhTM suppressed the mRNA expression of heme oxygenase-1, plasminogen activator inhibitor type-1, tissue factors, and inflammatory cytokines compared with the control group. rhTM did not change the hepatic GSH content at 2 h after APAP injection, but restored them at 4 h after the insult. rhTM ameliorated liver damage in mice with AILI, probably via the improvement in liver perfusion induced by it's anticoagulant acitivity, which can lead to the suppression of secondary liver damage.

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Section: Resultsmentioning

confidence: 91%

Section: Methodsmentioning

confidence: 99%

Recombinant human soluble thrombomodulin ameliorates acetaminophen‑induced liver toxicity in mice

et al. 2019

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“…Adolescent amphetamine disruption of adult hippocampal plasticity is also dependent on pleiotrophin [ 134 ]. Some of these effects may be involved in the neurotoxic effects of these drugs as well [ 135 – 137 ].…”

Section: Synaptic Camsmentioning

confidence: 99%

The Role of Cell Adhesion Molecule Genes Regulating Neuroplasticity in Addiction

2018

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A variety of genetic approaches, including twin studies, linkage studies, and candidate gene studies, has established a firm genetic basis for addiction. However, there has been difficulty identifying the precise genes that underlie addiction liability using these approaches. This situation became especially clear in genome-wide association studies (GWAS) of addiction. Moreover, the results of GWAS brought into clarity many of the shortcomings of those early genetic approaches. GWAS studies stripped away those preconceived notions, examining genes that would not previously have been considered in the study of addiction, consequently creating a shift in our understanding. Most importantly, those studies implicated a class of genes that had not previously been considered in the study of addiction genetics: cell adhesion molecules (CAMs). Considering the well-documented evidence supporting a role for various CAMs in synaptic plasticity, axonal growth, and regeneration, it is not surprising that allelic variation in CAM genes might also play a role in addiction liability. This review focuses on the role of various cell adhesion molecules in neuroplasticity that might contribute to addictive processes and emphasizes the importance of ongoing research on CAM genes that have been implicated in addiction by GWAS.

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“…Furthermore, a periadolescent amphetamine treatment was found to produce transient cognitive deficits only in PTN-/-mice, not in wild type (WT) mice (Gramage et al, 2013a). Interestingly, amphetamine-induced neurotoxic effects in the nigrostriatal pathway are enhanced in PTN-/-mice compared to WT mice (Gramage et al, 2010b;Soto-Montenegro et al, 2015). Also, it has to be noted that amphetamine-induced increase of GFAP-positive astrocytes, a hallmark of the neuroinflammation induced by this type of psychostimulants, was slightly increased in the striatum of PTN-/-mice (Gramage et al, 2010a).…”

Section: Introductionmentioning

confidence: 99%

Pleiotrophin overexpression regulates amphetamine-induced reward and striatal dopaminergic denervation without changing the expression of dopamine D1 and D2 receptors: Implications for neuroinflammation

Vicente-Rodríguez

Gonzalez

Gramage

et al. 2016

European Neuropsychopharmacology

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Functional neuroimaging of amphetamine-induced striatal neurotoxicity in the pleiotrophin knockout mouse model

Cited by 7 publications

References 38 publications

Recombinant human soluble thrombomodulin ameliorates acetaminophen‑induced liver toxicity in mice

Recombinant human soluble thrombomodulin ameliorates acetaminophen‑induced liver toxicity in mice

The Role of Cell Adhesion Molecule Genes Regulating Neuroplasticity in Addiction

Pleiotrophin overexpression regulates amphetamine-induced reward and striatal dopaminergic denervation without changing the expression of dopamine D1 and D2 receptors: Implications for neuroinflammation

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