Nitric Oxide Regulates Neurogenesis in the Hippocampus following Seizures.
Nitric Oxide Regulates Neurogenesis in the Hippocampus following Seizures.
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DOI：
10.1155/2015/451512
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发表时间：
2015
影响因子：
--
通讯作者：
Araújo IM
中科院分区：
文献类型：
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作者：
Carreira BP;Santos DF;Santos AI;Carvalho CM;Araújo IM
海马神经发生因脑损伤而改变。当神经炎症伴损伤时，驻留的小胶质细胞的激活促进炎症细胞因子和活性氧/氮物质如一氧化氮（NO）的释放。在这些条件下，NO促进海马神经干细胞（NSC）的增殖。然而，一氧化氮在损伤齿状回新生细胞的存活和分化中的作用尚不清楚。本研究采用kainic acid （KA）诱导的小鼠癫痫模型，研究了NO在癫痫发作后对海马中NSC增殖、迁移、分化和存活的调控作用。我们发现，一氧化氮增加了癫痫发作后NSC的增殖和神经母细胞的数量，但不利于新生神经元的存活。一氧化氮也是维持长期神经炎症所必需的。综上所述，我们的数据表明，一氧化氮对癫痫发作后神经发生的初始阶段有积极作用，但会损害新生神经元的存活。
Hippocampal neurogenesis is changed by brain injury. When neuroinflammation accompanies injury, activation of resident microglial cells promotes the release of inflammatory cytokines and reactive oxygen/nitrogen species like nitric oxide (NO). In these conditions, NO promotes proliferation of neural stem cells (NSC) in the hippocampus. However, little is known about the role of NO in the survival and differentiation of newborn cells in the injured dentate gyrus. Here we investigated the role of NO following seizures in the regulation of proliferation, migration, differentiation, and survival of NSC in the hippocampus using the kainic acid (KA) induced seizure mouse model. We show that NO increased the proliferation of NSC and the number of neuroblasts following seizures but was detrimental to the survival of newborn neurons. NO was also required for the maintenance of long-term neuroinflammation. Taken together, our data show that NO positively contributes to the initial stages of neurogenesis following seizures but compromises survival of newborn neurons.