Adenosine A1 receptor activates background potassium channels and modulates information processing in olfactory bulb mitral cells
Adenosine A1 receptor activates background potassium channels and modulates information processing in olfactory bulb mitral cells
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DOI：
10.1113/jp275503
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发表时间：
2017-12
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通讯作者：
Natalie Rotermund;Svenja Winandy;Timo Fischer;Kristina Schulz;T. Fregin;Nadine Alstedt;Melanie Buchta;Janick Bartels;M. Carlström;C. Lohr;Daniela Hirnet
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作者：
Natalie Rotermund;Svenja Winandy;Timo Fischer;Kristina Schulz;T. Fregin;Nadine Alstedt;Melanie Buchta;Janick Bartels;M. Carlström;C. Lohr;Daniela Hirnet
腺苷是一种广泛存在于哺乳动物脑中的神经调质，但它是否影响感觉系统的信息处理仍不清楚。在这里，我们表明，腺苷A1受体hyperglycemia二尖瓣细胞，一类主要的神经元，传播气味信息从嗅球到更高的大脑区域，通过激活背景K+通道。腺苷调节的背景K+通道属于双孔结构域K+通道家族。腺苷减少二尖瓣细胞的自发活动，而刺激感觉神经元时突触输入诱发的动作电位放电不受影响，导致诱发放电（信号）与自发放电（噪声）的比率更高，因此信噪比改善。该研究首次表明，腺苷影响感觉系统中输入-输出关系的微调。
Adenosine is a widespread neuromodulator in the mammalian brain, but whether it affects information processing in sensory system(s) remains largely unknown. Here we show that adenosine A1 receptors hyperpolarize mitral cells, one class of principal neurons that propagate odour information from the olfactory bulb to higher brain areas, by activation of background K+ channels. The adenosine‐modulated background K+ channels belong to the family of two‐pore domain K+ channels. Adenosine reduces spontaneous activity of mitral cells, whereas action potential firing evoked by synaptic input upon stimulation of sensory neurons is not affected, resulting in a higher ratio of evoked firing (signal) over spontaneous firing (noise) and hence an improved signal‐to‐noise ratio. The study shows for the first time that adenosine influences fine‐tuning of the input–output relationship in sensory systems.