Dr. Diering and his colleagues then searched for the molecular trigger for this change. They found that hundreds of proteins increase or decrease inside of synapses during the night. But one protein in particular, called Homer1A, stood out.
迪林博士和同事们随后开始寻找这种变化的分子触发因素。他们发现,在突触内,有数百种蛋白质在夜间增加或减少。但有一种名为Homer1A的蛋白质格外突出。
In earlier experiments on neurons in a dish, Homer1A proved to be important for paring back synapses. Dr. Diering wondered if it was important in sleep, too.
在对神经元进行的早期实验室实验中,Homer1A被证明在突触减少过程中发挥了重要作用。迪林博士想知道它是否在睡眠中也很重要。
To find out, he and his colleagues studied mice genetically engineered so that they couldn’t make Homer1A proteins. These mice slept like ordinary mice, but their synapses didn’t change their proteins like the ones in ordinary mice.
为了发现这一点,他和同事研究了经基因工程改造、不能制造Homer1A蛋白的小鼠。这些小鼠可以像普通小鼠一样睡觉,但是它们的突触不像在普通小鼠中那样改变其蛋白质。
Dr. Diering’s research suggests that sleepiness triggers neurons to make Homer1A and ship it into their synapses. When sleep arrives, Homer1A turns on the pruning machinery.
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