In adult mammals, including humans, the subventricular zone （SVZ） of the lateral ventricles and the subgranular zone of the dentate gyms （DG） show ongoing neurogenesis. Cerebral ischemic insults trigger neurogenes...In adult mammals, including humans, the subventricular zone （SVZ） of the lateral ventricles and the subgranular zone of the dentate gyms （DG） show ongoing neurogenesis. Cerebral ischemic insults trigger neurogenesis from neural stem cells or progenitor cells located in the SVZ and DG. Newborn neurons are then functionally recruited into the circuitry of the CA1 region, striatum and DG granule cell layer.展开更多
Objective It has been reported that B-cell lymphoma 2 （Bcl-2） enhances neurogenesis as well as supporting axonal growth after injury. In the present study, we investigated whether Bcl-2 overexpression plays a role i...Objective It has been reported that B-cell lymphoma 2 （Bcl-2） enhances neurogenesis as well as supporting axonal growth after injury. In the present study, we investigated whether Bcl-2 overexpression plays a role in the formation of newborn striatonigral projection neurons in the adult rat brain after transient middle cerebral artery occlusion （MCAO）. Methods We infused human Bcl-2-expressing plasmid （pBcl-2） into the lateral ventricle immediately after 30 min of MCAO, injected 5＇-bromodeoxyuridine （BrdU） intraperitoneally to label proliferative cells, and microinjected fluorogold （FG） into the substantia nigra at 11 weeks of reperfusion followed by multiple immunostaining of striatonigral projection neurons at 12 weeks. Results We found that pBcl-2 treatment significantly increased the number of newborn neurons （BrdU＋-NeuN＋） in the striatum ipsilateral to the MCAO. We further detected newborn striatonigral projection neurons （BrdU＋-FG＋-NeuN＋） in the ipsilateral striatum at 12 weeks. More interestingly, the number of newborn striatonigral projection neurons （BrdU＋-FG＋） was significantly increased by pBcl-2 treatment compared to that by pEGFP, a control plasmid. Conclusion Taken together, we found that Bcl-2 overexpression in the brain enhanced the generation of newborn striatonigral projection neurons. This provides a potential strategy for promoting the reestablishment of neural networks and brain repair after ischemic injury.展开更多
文摘In adult mammals, including humans, the subventricular zone （SVZ） of the lateral ventricles and the subgranular zone of the dentate gyms （DG） show ongoing neurogenesis. Cerebral ischemic insults trigger neurogenesis from neural stem cells or progenitor cells located in the SVZ and DG. Newborn neurons are then functionally recruited into the circuitry of the CA1 region, striatum and DG granule cell layer.
基金supported by grants from the National Basic Research Development Program of China (2006CB504100 and 2006CB943702)the National Natural Science Foundation of China(81030020 and J0730860)
文摘Objective It has been reported that B-cell lymphoma 2 （Bcl-2） enhances neurogenesis as well as supporting axonal growth after injury. In the present study, we investigated whether Bcl-2 overexpression plays a role in the formation of newborn striatonigral projection neurons in the adult rat brain after transient middle cerebral artery occlusion （MCAO）. Methods We infused human Bcl-2-expressing plasmid （pBcl-2） into the lateral ventricle immediately after 30 min of MCAO, injected 5＇-bromodeoxyuridine （BrdU） intraperitoneally to label proliferative cells, and microinjected fluorogold （FG） into the substantia nigra at 11 weeks of reperfusion followed by multiple immunostaining of striatonigral projection neurons at 12 weeks. Results We found that pBcl-2 treatment significantly increased the number of newborn neurons （BrdU＋-NeuN＋） in the striatum ipsilateral to the MCAO. We further detected newborn striatonigral projection neurons （BrdU＋-FG＋-NeuN＋） in the ipsilateral striatum at 12 weeks. More interestingly, the number of newborn striatonigral projection neurons （BrdU＋-FG＋） was significantly increased by pBcl-2 treatment compared to that by pEGFP, a control plasmid. Conclusion Taken together, we found that Bcl-2 overexpression in the brain enhanced the generation of newborn striatonigral projection neurons. This provides a potential strategy for promoting the reestablishment of neural networks and brain repair after ischemic injury.
