【摘要】 主要嗅觉表皮组织(MOE)是哺乳动物感知气味分子的重要器官,气味诱导是嗅觉受体神经元(ORN)活动的起点,嗅觉受体(OR)结合气味分子后通过环腺苷酸(c AMP)信号通路向下游传递信号。腺苷酸环化酶3(AC3)是此通路中的重要分子。为了探讨AC3缺失对小鼠MOE内ORs基因表达的影响,本文以AC3敲除型小鼠(AC3-/-)和野生型小鼠(AC3+/+)为材料,采用荧光定量PCR(qRT-PCR)、荧光原位杂交(FISH)技术分析了部分ORs基因及与其相关因子在MOE中的表达。qRT-PCR表明,3月龄AC3-/-小鼠MOE中嗅觉受体Olfr15、Olfr16、Olfr533、Olfr536、Olfr1507和Olfr642的表达量均显著下降。出生后PND7、PND30和PND90三个不同发育时期的AC3-/-小鼠MOE原位杂交显示,嗅觉受体Olfr15、Olfr536和Olfr1507表达的细胞数目均减少。进一步qRTPCR分析发现,3月龄AC3-/-小鼠嗅觉受体相关因子Rtp1、Rtp2、Reep1、Lhx2、Emx2和Ric-8b的表达也均发生显著下调。由此推测,AC3缺失导致的ORs及其相关因子的表达下调可能是嗅觉行为障碍的原因之一。更多还原

【Abstract】 Main olfactory epithelium（ MOE） is a primary organ for odorant detection.The odour sensing signaling is induced by odorant binding to odorant receptors（ ORs） and then sequentially launches the c AMP signal pathway.Adenylyl cyclase 3（AC3） is an important component of the olfactory c AMP signal pathway.In the present study,we used fluorogenic quantitative PCR and in situ hybridization approaches to study the expression of Olfr15,Olfr16,Olfr533,Olfr536,Olfr1507 and Olfr642 in MOEs of AC3 knock-out( AC3^-/- ) and wild-type(AC3^+/+) mice of different ages,and found that it is significantly down-regulated in MOEs of AC3^-/- mice.Furthermore,the expression of transcription factors,Lhx2 and Emx2,transport proteins,Rtp1 and Rtp2,and coupling G protein cofactor,Ric-8 b,is also significantly down-regulated in MOEs of AC3^-/- mice.Thus,we speculate that the down regulation of ORs and the related transcription factors in AC3^-/- mice may lead to defective olfactory detection.更多还原