1. Blockade of L-type voltage-gated Ca2+ channel inhibits ischemia-induced neurogenesis by down-regulating iNOS expression in adult mouse
- Author
-
Wei Wang, Ai Xia Zhang, Jin Sun, Shu Gang Zhang, Xiao Min Yang, Dong-Ya Zhu, Xiao Han, Chun Xia Luo, Xin Jian Zhu, Shu Hong Liu, and Youming Lu
- Subjects
medicine.medical_specialty ,biology ,business.industry ,Dentate gyrus ,Neurogenesis ,Central nervous system ,Hippocampus ,Subventricular zone ,Biochemistry ,Nitric oxide synthase ,Cellular and Molecular Neuroscience ,medicine.anatomical_structure ,Endocrinology ,nervous system ,Internal medicine ,biology.protein ,Medicine ,Artery occlusion ,Neuron ,business ,Neuroscience - Abstract
Neurogenesis in the adult mammalian hippocampus may contribute to repairing the brain after injury. The signals that regulate neurogenesis in the dentate gyrus following ischemic stroke insult are not well known. We have previously reported that inducible nitric oxide synthase (iNOS) expression is necessary for ischemia-stimulated neurogenesis in the adult dentate gyrus. Here, we show that mice subjected to 90 min of middle cerebral artery occlusion (MCAO) significantly increased the number of new neurons and up-regulated iNOS expression in the dentate gyrus. Blockade of the L-type voltage-gated Ca(2+) channel (L-VGCC) prevented neurogenesis in the dentate gyrus and subventricular zone (SVZ), and down-regulated iNOS expression in the dentate gyrus after cerebral ischemia. This study suggests that Ca(2+) influx through L-VGCC is involved in ischemia-induced neurogenesis by up-regulating iNOS expression.
- Published
- 2005