Mice lacking synapsin III show abnormalities in explicit memory and conditioned fear.
Mice lacking synapsin III show abnormalities in explicit memory and conditioned fear.
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DOI：
10.1111/j.1601-183x.2009.00555.x
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发表时间：
2010-04
期刊：
影响因子：
--
通讯作者：
Wetsel WC
中科院分区：
文献类型：
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作者：
Porton B;Rodriguiz RM;Phillips LE;Gilbert JW 4th;Feng J;Greengard P;Kao HT;Wetsel WC
突触蛋白III是一种神经元特异性磷蛋白，在突触传递和神经发育中起重要作用。虽然突触蛋白III在胚胎脑中丰富，但该蛋白在成人中的表达减少，主要限于海马体、嗅球和大脑皮层。鉴于突触蛋白III对这些脑区的特异性，并且由于它在齿状回的神经发生中起作用，我们研究了它是否可能影响小鼠的学习和记忆过程。为了解决这一点，突触蛋白III敲除小鼠在一般行为筛选，几个测试，以评估学习和记忆功能，和条件性恐惧。突变动物在感觉和运动功能或焦虑和抑郁样行为方面没有表现出异常。虽然突变体在Morris水迷宫中表现出轻微的变化，他们缺乏对象识别24小时和10天后的培训和社会传播的食物偏好在20分钟和24小时。此外，突变体显示异常反应的上下文和线索恐惧条件反射测试后1或24小时条件反射。突触蛋白III基因敲除的小鼠在恐惧增强的惊吓中也表现出异常反应。由于突触蛋白III蛋白在精神分裂症的大脑中减少，并且因为突变小鼠没有明显的解剖缺陷或神经系统疾病，这些突变体可能代表了一种独特的神经发育模型，用于解剖与精神分裂症和相关疾病的某些方面相关的分子途径。
Synapsin III is a neuron-specific phosphoprotein that plays an important role in synaptic transmission and neural development. While synapsin III is abundant in embryonic brain, expression of the protein in adults is reduced and limited primarily to the hippocampus, olfactory bulb, and cerebral cortex. Given the specificity of synapsin III to these brain areas and because it plays a role in neurogenesis in the dentate gyrus, we investigated whether it may affect learning and memory processes in mice. To address this point, synapsin III knockout mice were examined in a general behavioral screen, several tests to assess learning and memory function, and conditioned fear. Mutant animals displayed no anomalies in sensory and motor function or in anxiety- and depressive-like behaviors. Although mutants showed minor alterations in the Morris water maze, they were deficient in object recognition 24 hr and 10 days after training and in social transmission of food preference at 20 min and 24 hr. Additionally, mutants displayed abnormal responses in contextual and cued fear conditioning when tested 1 or 24 hr after conditioning. The synapsin III knockout mice also showed aberrant responses in fear-potentiated startle. Since synapsin III protein is decreased in schizophrenic brain and because the mutant mice do not harbor obvious anatomical deficits or neurological disorders, these mutants may represent a unique neurodevelopmental model for dissecting the molecular pathways that are related to certain aspects of schizophrenia and related disorders.