Neurogenesis, inflammation and behavior.
Neurogenesis, inflammation and behavior.
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DOI：
10.1016/j.bbi.2012.09.003
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发表时间：
2013-01
影响因子：
15.1
通讯作者：
Rhodes, Justin S.
中科院分区：
文献类型：
--
作者：
Kohman, Rachel A.;Rhodes, Justin S.
在20世纪90年代之前，人们普遍认为成年人的大脑无法再生神经元。然而，现在已经确定，新的神经元在海马和嗅球的齿状回中持续产生。成人神经发生的功能意义尚不清楚，但人们普遍认为，新的神经元有助于学习和记忆和/或通过取代死亡或垂死的细胞来维持大脑区域。已知许多不同的因素调节成人神经发生，包括免疫反应和大脑中免疫细胞释放的信号分子。虽然免疫激活（即，小胶质细胞的扩大、细胞因子的释放）通常被视为有害事件，免疫激活对神经功能的影响高度依赖于免疫应答的形式，因为脑中的小胶质细胞和其他免疫反应性细胞可以根据细胞的表型和行为支持或破坏脑功能。例如，表达炎性表型的小胶质细胞通常减少细胞增殖、存活和新神经元的功能，而显示替代保护性表型的小胶质细胞支持成年神经发生。本综述总结了目前对新神经元在认知和行为中的作用的认识，重点是免疫系统在炎症发作和健康未受伤大脑中影响成年海马神经发生的能力。已经提出，一些与炎症相关的认知缺陷可能部分与炎症诱导的成年海马神经发生减少有关。阐明免疫系统如何促进成人神经发生的调节将有助于预测免疫激活对神经可塑性的影响，并可能有助于发现在慢性炎症条件下保护神经发生的治疗方法。
Before the 1990s it was widely believed that the adult brain was incapable of regenerating neurons. However, it is now established that new neurons are continuously produced in the dentate gyrus of the hippocampus and olfactory bulb throughout life. The functional significance of adult neurogenesis is still unclear, but it is widely believed that the new neurons contribute to learning and memory and/or maintenance of brain regions by replacing dead or dying cells. Many different factors are known to regulate adult neurogenesis including immune responses and signaling molecules released by immune cells in the brain. While immune activation (i.e., enlargement of microglia, release of cytokines) within the brain is commonly viewed as a harmful event, the impact of immune activation on neural function is highly dependent on the form of the immune response as microglia and other immune-reactive cells in the brain can support or disrupt brain function depending on the phenotype and behavior of the cells. For instance, microglia that express an inflammatory phenotype generally reduce cell proliferation, survival and function of new neurons whereas microglia displaying an alternative protective phenotype support adult neurogenesis. The present review summarizes current understanding of the role of new neurons in cognition and behavior, with an emphasis on the immune system’s ability to influence adult hippocampal neurogenesis during both an inflammatory episode and in the healthy uninjured brain. It has been proposed that some of the cognitive deficits associated with inflammation may in part be related to inflammation-induced reductions in adult hippocampal neurogenesis. Elucidating how the immune system contributes to the regulation of adult neurogenesis will help in predicting the impact of immune activation on neural plasticity and potentially facilitate the discovery of treatments to preserve neurogenesis in conditions characterized by chronic inflammation.
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影响因子：
4.2
作者：
Bachstetter, Adam D.;Morganti, Josh M.;Jernberg, Jennifer;Schlunk, Andrea;Mitchell, Staten H.;Brewster, Kaelin W.;Hudson, Charles E.;Cole, Michael J.;Harrison, Jeffrey K.;Bickford, Paula C.;Gemma, Carmelina
通讯作者：
Gemma, Carmelina
影响因子：
3.5
作者：
Clark, Peter J.;Brzezinska, Weronika J.;Puchalski, Emily K.;Krone, David A.;Rhodes, Justin S.
通讯作者：
Rhodes, Justin S.
影响因子：
3.5
作者：
Clark, Peter J.;Bhattacharya, Tushar K.;Miller, Daniel S.;Kohman, Rachel A.;DeYoung, Erin K.;Rhodes, Justin S.
通讯作者：
Rhodes, Justin S.
影响因子：
3.7
作者：
Amrein I;Dechmann DK;Winter Y;Lipp HP
通讯作者：
Lipp HP
影响因子：
3.4
作者：
Amrein, Irmgard;Isler, Karin;Lipp, Hans-Peter
通讯作者：
Lipp, Hans-Peter