Light Alcohol Consumption Promotes Early Neurogenesis Following Ischemic Stroke in Adult C57BL/6J Mice

Ischemic stroke is one of the leading causes of death and disability worldwide. Neurogenesis plays a crucial role in postischemic functional recovery. Alcohol dose-dependently affects the prognosis of ischemic stroke. We investigated the impact of light alcohol consumption (LAC) on neurogenesis under physiological conditions and following ischemic stroke. C57BL/6J mice (three months old) were fed with 0.7 g/kg/day ethanol (designed as LAC) or volume-matched water (designed as control) daily for eight weeks. To evaluate neurogenesis, the numbers of 5-bromo-2-deoxyuridine (BrdU)(+)/doublecortin (DCX)(+) and BrdU(+)/NeuN(+) neurons were assessed in the subventricular zone (SVZ), dentate gyrus (DG), ischemic cortex, and ischemic striatum. The locomotor activity was determined by the accelerating rotarod and open field tests. LAC significantly increased BrdU(+)/DCX+ and BrdU(+)/NeuN(+) cells in the SVZ under physiological conditions. Ischemic stroke dramatically increased BrdU(+)/DCX+ and BrdU(+)/NeuN(+) cells in the DG, SVZ, ischemic cortex, and ischemic striatum. The increase in BrdU(+)/DCX+ cells was significantly greater in LAC mice compared to the control mice. In addition, LAC significantly increased BrdU(+)/NeuN(+) cells by about three folds in the DG, SVZ, and ischemic cortex. Furthermore, LAC reduced ischemic brain damage and improved locomotor activity. Therefore, LAC may protect the brain against ischemic stroke by promoting neurogenesis.