Expanded characterization of the social interaction abnormalities in mice lacking Dcl1
Expanded characterization of the social interaction abnormalities in mice lacking Dcl1
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DOI：
10.1046/j.1601-183x.2003.00045.x
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发表时间：
2004-02-01
影响因子：
2.5
通讯作者：
Wynshaw-Boris, A
中科院分区：
文献类型：
--
作者：
Long, JM;LaPorte, P;Wynshaw-Boris, A
Dvl1是在胚胎发育和成年中枢神经系统中广泛表达的三个小鼠蓬乱基因之一。杂乱的蛋白质是WRIT和平面细胞极性发育信号通路的必要组成部分。我们以前报道过Dvl1基因缺陷的小鼠表现出异常的社会互动和感觉运动门控。为了评估我们早期发现的有效性，我们重复了之前的行为测试，并包括了几种新的分析方法。评估的行为包括：社会互动、感觉运动反射、运动活动、伤害性感受、脉冲前抑制声惊厥(PPI)以及学习和记忆。带有明确社会成分的评估包括：社交优势测试、胡须修剪、筑巢、家庭笼子挤在一起和幼崽的超声波发音率分析。此外，还评估了野生型和Dvl1缺失型小鼠对同种小鼠的社会识别能力。复制最初的报告，Dvl1基因缺失的小鼠在几个包含明确社会成分的任务中受损。然而，在社会记忆任务中没有观察到损害。此前观察到的PPI逆差没有在两家机构重复出现。综上所述，我们提供的证据表明，Dvl1缺陷小鼠的社会交互表型具有很强的遗传影响，但感觉运动门控缺陷受环境影响。观察到的社会互动缺陷的特殊性也表明，Dvl1的缺乏与对社会等级和支配地位的认识不足有关。
Dvl1 is one of three murine Dishevelled genes widely expressed in embryonic development and in the adult central nervous system. Dishevelled proteins are a necessary component of the Writ and planar cell polarity developmental signaling pathways. We reported previously that mice deficient in Dvl1 exhibited abnormal social interaction and sensorimotor gating. To assess the validity of our earlier findings, we replicated the previous behavioral tests and included several new assays. The behaviors assessed included: social interaction, sensorimotor reflexes, motor activity, nociception, prepulse inhibition of acoustic startle (PPI) and learning and memory. Assessments with an explicit social component included: social dominance test, whisker trimming, nest building, home-cage huddling and ultrasonic vocalization rate analysis in pups. In addition, separate cohorts of wildtype and Dvl1-null mice were assessed for social recognition of a conspecific. Replicating the original report, Dvl1-null mice were impaired in several tasks containing an explicit social component. However, no impairment was observed in the social memory task. A previously observed deficit in PPI did not replicate in two institutions. In conclusion, we provide evidence that the social interaction phenotype of Dvl1-deficient mice has a strong genetic influence, but the sensorimotor gating deficit was subject to environmental influences. The specificity of observed social interaction deficits also suggests that lack of Dvl1 is associated with deficits in the recognition of social hierarchy and dominance.