Cognitive deficits induced by combined exposure of stress and alcohol mediated through oxidative stress-PARP pathway in the hippocampus. (13th July 2017)

• Record Type: Journal Article
• Authors: Pant, Rajat; Jangra, Ashok; Kwatra, Mohit; Singh, Tavleen; Kushwah, Pawan; Bezbaruah, Babul Kumar; Gurjar, Satendra Singh; Phukan, Swopna
• Is Part Of: Neuroscience letters. Volume 653(2017)
• Page Start: 208
• Page End: 214
• Publication Date: 2017-07-13
• Subjects: Alcohol -- Memory -- PARP -- Restraint stress -- Oxidative stress; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2017.05.058
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Restraint stress increases alcohol consumption in mice. Combined exposure of alcohol and stress aggravates memory deficits. Oxidative stress-PARP cascade gets activated in alcohol and stress-exposed mice. 1, 5-isoquinolinediol ameliorates alcohol and stress-induced memory deficits. Abstract: Several studies reported that stress can enhance the consumption of alcohol in humans and animals. However, the combinatorial effect of stress and alcohol on cognitive function and neurochemical alterations is quite understudied. In the present study, we have elucidated the involvement of oxidative stress-PARP cascade in alcohol and restraint stress (RS)-exposed animals using a PARP inhibitor, 1, 5-isoquinolinediol (3 mg/kg for 14 days). Male Swiss albino mice were given alcohol (ALC) or RS (2 h per day) or both in ALC + RS group for 28 days. Behavioral analysis revealed cognitive dysfunction in ALC + RS group. Furthermore, oxidative stress and raised level of pro-inflammatory cytokines were found in the hippocampus region of ALC + RS group. Semi-quantitative reverse transcriptase PCR showed overactivation of PARP-1 gene in ALC + RS group. 1, 5-isoquinolinediol treatment significantly prevented cognitive deficits and aforementioned neurochemical alterations. Overall, our findings showed that ALC + RS exerted deleterious effects on the hippocampus which involves oxidative stress-PARP overactivation cascade.