Modulation of Fgfr1a Signaling in Zebrafish Reveals a Genetic Basis for the Aggression-Boldness Syndrome
Modulation of Fgfr1a Signaling in Zebrafish Reveals a Genetic Basis for the Aggression-Boldness Syndrome
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DOI：
10.1523/jneurosci.2892-11.2011
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发表时间：
2011-09-28
影响因子：
5.3
通讯作者：
Bally-Cuif, Laure
中科院分区：
文献类型：
--
作者：
Norton, William H. J.;Stumpenhorst, Katharina;Bally-Cuif, Laure
行为综合症是两种或两种以上行为的组合，这些行为与环境相关。攻击性-大胆综合症将攻击性、大胆和在新环境中的探索活动联系在一起。尽管在许多动物身上都描述了大胆攻击的行为，但其行为成分之间的联系机制尚不清楚。在这里，我们展示了编码成纤维细胞生长因子受体1a(Fgfr1a)的基因突变同时增加了成年斑马鱼的攻击性、胆大性和探索性。我们证明改变的成纤维细胞生长因子信号也导致突变的脑组织胺水平降低。药理学上增加组胺信号足以挽救fgfr1a突变体的行为表型。总而言之，我们发现一个单一的基因位点可能是攻击性-大胆行为综合症的基础。我们还确定了可能调节这些行为聚集的神经递质途径之一。
Behavioral syndromes are suites of two or more behaviors that correlate across environmental contexts. The aggression-boldness syndrome links aggression, boldness, and exploratory activity in a novel environment. Although aggression-boldness has been described in many animals, the mechanism linking its behavioral components is not known. Here we show that mutation of the gene encoding fibroblast growth factor receptor 1a (fgfr1a) simultaneously increases aggression, boldness, and exploration in adult zebrafish. We demonstrate that altered Fgf signaling also results in reduced brain histamine levels in mutants. Pharmacological increase of histamine signaling is sufficient to rescue the behavioral phenotype of fgfr1a mutants. Together, we show that a single genetic locus can underlie the aggression-boldness behavioral syndrome. We also identify one of the neurotransmitter pathways that may mediate clustering of these behaviors.