Ischemia-induced glutamate release in rat frontoparietal cortex after chronic alcohol and withdrawal

Favalli, L.; Rozza, A.; Frattini, P.; Masoero, Elisabetta; Scelsi, R; Pascale, Alessia; Govoni, Stefano

doi:10.1016/s0304-3940(02)00352-x

Cited by 11 publications

(9 citation statements)

References 17 publications

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“…As biological confirmation of the identified transcriptional response, we therefore assessed brain damage following chronic EtOH exposure in both sexes. Brains were examined 10 days after withdrawal as the withdrawal process, and not EtOH exposure per se, plays a major role in alcohol-induced toxicity (Favalli et al, 2002). The 10-day time point was based on the time associated with neuronal damage following a prototypical excitotoxic insult (Panegyres, 1998), which is considered an important mediator of alcohol-induced brain damage (Harper and Matsumoto, 2005;Prendergast et al, 2004).…”

Section: Enhanced Alcohol-induced Brain Damage In Femalesmentioning

confidence: 99%

“…To quantify the effect of chronic EtOH withdrawal on brain damage in both sexes, we evaluated histopathology in the lateral parietal cortex. Parietal cortex as a region of interest offered the advantage that, in addition to PFC, it has also been shown to demonstrate damage in human alcoholics (Gazdzinski et al, 2005) and after EtOH withdrawal in rodents (Favalli et al, 2002). In addition, the lateral parietal cortex is part of the network involved in inhibitory control along with the PFC (Watanabe et al, 2002), is a discrete region as opposed to the PFC with seven cortical layers, and was also identified in a visual screen performed to assess brain regions demonstrating neuronal damage.…”

Section: Enhanced Alcohol-induced Brain Damage In Femalesmentioning

confidence: 99%

“…Estimates suggest that 4-7% of alcoholics suffer from seizures (Hauser, 1990). In addition, withdrawal likely plays a major role in alcohol-induced neurotoxicity (Favalli et al, 2002). Finally, withdrawal severity has been shown to be inversely genetically correlated with alcohol consumption in animal models (Metten et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Neurotoxic Consequences of Chronic Alcohol Withdrawal: Expression Profiling Reveals Importance of Gender Over Withdrawal Severity

Hashimoto

Wiren

2007

Neuropsychopharmacol

111

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While women are more vulnerable than men to many of the medical consequences of alcohol abuse, the role of sex in the response to ethanol is controversial. Neuroadaptive responses that result in the hyperexcitability associated with withdrawal from chronic ethanol likely reflect gene expression changes. We have examined both genders for the effects of withdrawal on brain gene expression using mice with divergent withdrawal severity that have been selectively bred from a genetically heterogeneous population. A total of 295 genes were identified as ethanol regulated from each gender of each selected line by microarray analyses. Hierarchical cluster analysis of the arrays revealed that the transcriptional response correlated with sex rather than with the selected withdrawal phenotype. Consistent with this, gene ontology category over-representation analysis identified cell death and DNA/RNA binding as targeted classes of genes in females, while in males, protein degradation, and calcium ion binding pathways were more altered by alcohol. Examination of ethanolregulated genes and these distinct signaling pathways suggested enhanced neurotoxicity in females. Histopathological analysis of brain damage following ethanol withdrawal confirmed elevated cell death in female but not male mice. The sexually dimorphic response was observed irrespective of withdrawal phenotype. Combined, these results indicate a fundamentally distinct neuroadaptive response in females compared to males during chronic ethanol withdrawal and are consistent with observations that female alcoholics may be more vulnerable than males to ethanol-induced brain damage associated with alcohol abuse.

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Section: Enhanced Alcohol-induced Brain Damage In Femalesmentioning

confidence: 99%

Section: Enhanced Alcohol-induced Brain Damage In Femalesmentioning

confidence: 99%

See 1 more Smart Citation

Neurotoxic Consequences of Chronic Alcohol Withdrawal: Expression Profiling Reveals Importance of Gender Over Withdrawal Severity

Hashimoto

Wiren

2007

Neuropsychopharmacol

111

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“…10 In experimental studies, it has been described that chronic alcohol exposure increases excitotoxic/ischemic damage. [11][12][13][14] Surprisingly, to our knowledge, apart from 1 study dealing with intra-arterial thrombolysis, 15,16 no studies have to date examined the consequences of previous alcohol consumption on the benefits of intravenous thrombolysis after ischemic stroke. Thus, the aims of our study were (1) to evaluate, in a model of stroke, the influence of alcoholic history on the benefit/risk ratio of thrombolysis and (2) to determine the mechanisms sustaining this potential influence.…”

mentioning

confidence: 99%

Impact of Alcohol Consumption on the Outcome of Ischemic Stroke and Thrombolysis

Lemarchand

Gauberti

Lizarrondo

et al. 2015

Stroke

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Background and Purpose-Tissue-type plasminogen activator (tPA) is the only acute treatment for ischemic stroke.Unfortunately, the benefit of tPA-driven thrombolysis is not systematic, and understanding the reasons for this is mandatory. The balance between beneficial and detrimental effects of tPA might explain the limited overall efficiency of thrombolysis. Here, we investigated whether this balance could be influenced by excessive alcohol intake. Methods-We used a murine model of thromboembolic stroke, coupled to an array of biochemical assays, near-infrared or magnetic resonance imaging scans, 2-photon microscopy, hydrodynamic transfections, and immunohistological techniques. Results-We found that 6 weeks of alcohol consumption (10% in drinking water) worsens ischemic lesions and cancels the beneficial effects of tPA-induced thrombolysis. We accumulate in vivo and in vitro evidence showing that this aggravation is correlated with a decrease in lipoprotein receptor-related protein 1-mediated hepatic clearance of tPA in alcoholexposed mice. Conclusions-An efficient liver-driven clearance of tPA might influence the safety of thrombolysis after stroke.

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“…

IntroductionExcitotoxicity, one important determinant in various diseases of the central nervous system (CNS), is involved in acute ischemic brain injury [1][2][3] and can initiate postischemic inflammation by inducing the expression of pro-inflammatory molecules/mediators [4][5][6] . Mediators in postischemic inflammation include 5-lipoxygenase (5-LOX) metabolites eg, cysteinyl leukotrienes (CysLT, including LTC 4 , LTD 4 and LTE 4 ) [7][8][9][10][11] .

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mentioning

confidence: 99%

Cysteinyl leukotriene receptor 1 is involved in N-methyl-D-aspartate-mediated neuronal injury in mice

Ding

Wei

Zhang

et al. 2006

Acta Pharmacologica Sinica

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Aim: To determine whether cysteinyl leukotriene receptor 1 (CysLT1 receptor) is involved in N‐methyl‐D‐aspartate (NMDA)‐induced excitotoxic injury in the mouse brain. Methods: Brain injury was induced by NMDA microinjection (50‐150 nmol in 0.5 uL) into the cerebral cortex. The changes in CysLT1 receptor expression 24 h after NMDA injection and the effects of a CysLT2 receptor antagonist, pranlukast (0.01 and 0.1 mg/kg), an NMDA receptor antagonist, ketamine (30 mg/kg), and an antioxidant, edaravone (9 mg/kg) were observed. Results: In the NMDA‐injured brain, the CysLT1 receptor mRNA, and protein expression were upregulated, and the receptor was mainly localized in the neurons and not in the astrocytes. Pranlukast, ketamine and edaravone decreased NMDA‐induced injury; pranlukast (0.1 mg/kg) and ketamine inhibited the upregulated expression of the CysLT1 receptor. Conclusion: CysLT1 receptor expression in neurons is upregulated after NMDA injection, and NMDA‐induced responses are inhibited by CysLT1 receptor antagonists, indicating that the increased CysLT1 receptor is involved in NMDA excitotoxicity.

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Ischemia-induced glutamate release in rat frontoparietal cortex after chronic alcohol and withdrawal

Cited by 11 publications

References 17 publications

Neurotoxic Consequences of Chronic Alcohol Withdrawal: Expression Profiling Reveals Importance of Gender Over Withdrawal Severity

Neurotoxic Consequences of Chronic Alcohol Withdrawal: Expression Profiling Reveals Importance of Gender Over Withdrawal Severity

Impact of Alcohol Consumption on the Outcome of Ischemic Stroke and Thrombolysis

Cysteinyl leukotriene receptor 1 is involved in N-methyl-D-aspartate-mediated neuronal injury in mice

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