Abstract

Chronic consumption of ethanol has a damaging effect in various organs and metabolic functions, including liver, kidney, heart, pancreas, and brain (Sun and Sun, 2001; Bezerra Rde et al., 2005). Additionally, it has been shown that both the acute and chronic ethanol intake induce alteration in voltage-gated channels causing behavioral and electrophysiological changes in the brain (Little, 1999). In the last few years, the effect of ethanol in the electrophysiological phenomenon, known as cortical spreading depression (CSD), has been widely assessed (Sonn and Mayevsky, 2001; Bezerra Rde et al., 2005; Abadie-Guedes et al., 2008) as an important model to predict the damaging effects of ethanol in both young and aged brains.

Highlights

  • Cortical spreading depression is a neuronal and glial depolarization wave in gray matter, which is thought to be associated as an upstream event in migraine with aura, spontaneous intracerebral hemorrhage, ischemic injury and brain trauma (Zhou et al, 2010; Dreier, 2011)

  • Chronic ethanol administration affects the antioxidant defenses of the brain by reducing the levels of glutathione, peroxidase, α -tocopherol, glutathione reductase and catalase (Bezerra Rde et al, 2005), and the aged brain is affected by this reduced antioxidant scavenging system (Reiter, 1995)

  • Astrocytes have been shown to be more resistant than neurons during ethanol-induced oxidative stress because of their greater content of glutathione (GSH) and other antioxidant enzymes (Watts et al, 2005; Barreto et al, 2011), and these cells may play an important role in cortical spreading depression (CSD)

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Summary

Introduction

Cortical spreading depression is a neuronal and glial depolarization wave in gray matter, which is thought to be associated as an upstream event in migraine with aura, spontaneous intracerebral hemorrhage, ischemic injury and brain trauma (Zhou et al, 2010; Dreier, 2011). One of the main mechanisms of ethanol-induced brain damage is due to an augmented production of reactive oxygen species (ROS), leading to increased CSD propagation, this statement has not been experimentally addressed.

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