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Mechanisms of formation, maintenance and extinction of olfactory learning

嗅觉学习的形成、维持和消退机制

基本信息

批准号：
13480268
负责人：
KABA Hideto
金额：
$ 9.54万
依托单位：
Kochi University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2003
项目状态：
已结题

项目摘要

Female mice learn to recognize the urinary pheromones of the male with which they mate. This olfactory learning is associated with substantial neural changes in the accessory olfactory bulb(AOB), first relay in the vomeronasal system. We show in AOB slices that glutamatergic transmission from mitral cells, a single class of projection neurons, to granule cell inhibitory interneurons, displays long-term potentiation(LTP), which shares essential features with pheromonal learning, following spaced and long-term theta frequency stimulation of mitral cell axons and that noradrenaline enhances the induction of LTP via presynaptic α_2-adrenergic receptor-mediated inhibition of glutamate release that allows the postsynaptic cell to fire more action potentials during theta frequency stimulus train due to a reduction in depolarising plateau. Our findings provide a unique cellular mechanism for the noradrenergic modulation of olfactory learning.On postnatal day 12, young rats show an aversion to an odor to which they has been exposed along with presentation of foot shock on postnatal day 11. We show that the mitogen-activated protein kinase/extracellular-signal regulated kinase(MAPK/ERK)-cyclic AMP response element binding protein(CREB) pathway in the olfactory bulb(OB) is required for the long-term, but not the short-term, facilitation process of aversive olfactory learning in young rats. We also show that both of GABA_A and GABA_B reeptors in the OB are involved in the regulation of aversive olfactory learning.

雌鼠学会识别与之交配的雄鼠的尿液信息素。这种嗅觉学习与副嗅球（AOB）中的大量神经变化相关，首先在犁鼻系统中中继。我们在AOB切片中表明，从僧帽细胞（一类投射神经元）到颗粒细胞抑制性中间神经元的谷氨酸能传递显示出长时程增强（LTP），这与信息素学习具有共同的基本特征，在间隔和长时间θ频率刺激二尖瓣细胞轴突后，去甲肾上腺素通过突触前α_2-肾上腺素能受体增强LTP的诱导。介导的谷氨酸释放抑制，其允许突触后细胞在θ频率刺激序列期间由于去极化平台的减少而激发更多的动作电位。我们的研究结果提供了一个独特的细胞机制去甲肾上腺素调节嗅觉learning.On postnatal days 12，年轻的大鼠表现出厌恶的气味，他们已被暴露沿着与介绍足休克在postnatal days 11。我们发现，有丝分裂原活化蛋白激酶/细胞外信号调节激酶（MAPK/ERK）-环磷酸腺苷反应元件结合蛋白（CREB）通路在嗅球（OB）所需的长期，而不是短期，促进过程中的厌恶嗅觉学习在年轻的大鼠。我们还发现，嗅球中的GABA_A和GABA_B受体都参与了厌恶性嗅觉学习的调节。