美國密歇根大學(xué)的哈維爾·佩雷斯等人在《神經(jīng)科學(xué)雜志》上介紹說(shuō)，他們通過(guò)篩選法培育出兩類(lèi)大鼠，一類(lèi)焦慮不安，一類(lèi)比較安定，檢測發(fā)現，焦慮不安的大鼠與安定的大鼠相比，前者大腦中的成纖維細胞生長(cháng)因子2（簡(jiǎn)稱(chēng)FGF2）水平較低。
佩雷斯說(shuō)，改善焦慮不安大鼠的外部生存環(huán)境，比如給它們大的居住空間或者給它們一些玩具，可提高它們大腦中FGF2的水平，并減輕它們的焦慮情緒。
佩雷斯說(shuō)：“此前人們知道FGF2與大腦發(fā)育有關(guān)，可幫助修復大腦創(chuàng )傷，但我們發(fā)現，FGF2還扮演了另外兩個(gè)重要角色：它是導致焦慮癥的遺傳因素，也是環(huán)境影響人體的調節因素，這讓人非常驚訝。”（生物谷Bioon.com）
生物谷推薦原始出處：
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.
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