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美国研究人员5月12日说，动物试验表明，一种与大脑发育有关的化学物质或许可帮助减轻焦虑症甚至抑郁症。 美国密歇根大学的哈维尔·佩雷斯等人在《神经科学杂志》上介绍说，他们通过筛选法培育出两类大鼠，一类焦虑不安，一类比较安定，检测发现，焦虑不安的大鼠与安定的大鼠相比，前者大脑中的成纤维细胞生长因子2（简称FGF2）水平较低。 佩雷斯说，改善焦虑不安大鼠的外部生存环境，比如给它们大的居住空间或者给它们一些玩具，可提高它们大脑中FGF2的水平，并减轻它们的焦虑情绪。 佩雷斯说：“此前人们知道FGF2与大脑发育有关，可帮助修复大脑创伤，但我们发现，FGF2还扮演了另外两个重要角色：它是导致焦虑症的遗传因素，也是环境影响人体的调节因素，这让人非常惊讶。” 推荐原始出处： The Journal of Neuroscience, May 13, 2009, doi:10.1523/JNEUROSCI.4829-08.2009 A New Role for FGF2 as an Endogenous Inhibitor of Anxiety Javier A. Perez, Sarah M. Clinton, Cortney A. Turner, Stanley J. Watson, and Huda Akil 1 Molecular and Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, Michigan 48109 Human postmortem studies have demonstrated that fibroblast growth factor-2 (FGF2) expression is decreased in the brain of depressed individuals. It remained unclear, however, whether this is a consequence of the illness or whether FGF2 plays a primary role in the control of mood and emotions. In this series of studies, we first ask whether endogenous FGF2 expression correlates with spontaneous anxiety, a trait associated with vulnerability to severe mood disorders in humans. This is tested in two genetically distinct groups of rats selectively bred to differ dramatically in their response to novelty and anxiety-provoking conditions (HRs = low anxiety/high response to novelty vs LRs = high anxiety/low response to novelty). We demonstrate that high-anxiety LRs have significantly lower levels of hippocampal FGF2 mRNA relative to low-anxiety HRs. We then demonstrate that FGF2 expression is modifiable by environmental factors that alter anxiety—thus, environmental complexity reduces anxiety behavior and induces FGF2 expression in hippocampus, particularly in high-anxiety LRs. Finally, we directly test the role of FGF2 as an anxiolytic and show that a 3 week treatment regimen of peripherally administered FGF2 is highly effective at blunting anxiety behavior, specifically in high-anxiety LRs. This treatment is accompanied by an increase in survival of adult-born hippocampal cells, both neurons and astrocytes, most clearly in LRs. These findings implicate hippocampal FGF2 as a central integrator of genetic and environmental factors that modify anxiety, point to hippocampal neurogenesis and gliogenesis as key in this modulation, and underscore FGF2's potential as a new target for treatment of depression and anxiety disorders. (责任编辑：Doctor001) |
