時(shí)差N小時(shí):失去知覺之后 Out for the Count

If you've ever had major surgery, you probablyremember lying down and waking up-but nothing inbetween.

如果你曾經(jīng)做過重大手術(shù)，那么你肯定只記得躺下去和醒來這么2個(gè)動(dòng)作，而其間過程是渾然不知的。

Thanks to the anesthesiologist, during the actualsurgery you were out of it: immobilized andinsensitive to pain.

多虧了麻醉師，你才能在手術(shù)中無知覺地度過：不能動(dòng)彈，也感覺不到疼痛。

But until recently scientists had little understandingof how anesthetics actually work on the cellular level.

但是直到最近科學(xué)家們才多少了解到麻醉藥是如何在細(xì)胞層面上工作的。

That's changed thanks to recent experiments performed by researchers at the University ofZurich, in Switzerland.

還得感謝瑞士蘇黎世大學(xué)的研究員們最近做的實(shí)驗(yàn)，這一困惑才得以解開。

They knew that anesthetics caused pain receptors in the brain to turn off by acting like mostdrugs do:

他們弄清楚了麻藥是通 過關(guān)閉大腦中的疼痛接收器才使人感覺不到疼痛，原理跟大多數(shù)藥物一樣：

anesthetizing drugs attach to particular sites on nerve cells and turn them off.

麻藥附著在神經(jīng)細(xì)胞上某個(gè)特殊位置，然后將感知功能關(guān)閉。

The question was, where on nerve cells do these drugs attach?

問題是，麻藥到底附著在什么位置呢?

Nerve cell membranes have receptors for different kinds of chemicals produced by the brain.

神經(jīng)細(xì)胞膜有多個(gè)接收器來識(shí)別大腦產(chǎn)生的不同類別的化學(xué)物質(zhì)。

Gamma-amino butyric acid, or GABA, for example, is a chemical that shuts down nerve cells.

例如γ-氨基丁酸，或者簡(jiǎn)寫為GABA，就是可以關(guān)閉神經(jīng)細(xì)胞感知功能的化學(xué)物質(zhì)。

The hypothesis was that general anesthesia works by binding to GABA receptors on a nervecell,thereby activating the receptor and instructing the cell to shut down.

假設(shè)全身麻醉是將麻藥和在神經(jīng)細(xì)胞上的GABA接收器綁定在一起，從而激活接收器，然后再傳達(dá)閉接收功能的指令關(guān)閉。

So it made sense for the Zurich researchers to focus on GABA receptors.

這樣的假設(shè)就使蘇黎世大學(xué)的研究員們明白，集中精力研究GABA接收器是關(guān)鍵所在。

To do this they worked with mice that had been genetically engineered to have nerve cellswith GABA receptors that wouldn't respond to anesthetics.

為了證明這點(diǎn)，他們用基因改造過的老鼠做實(shí)驗(yàn)，這種老鼠身上的 GABA接收器對(duì)麻藥免疫。

And sure enough, when such mice were given anesthetic drugs they weren't nearly asimmune to pain as regular mice that had also been given pain-blocking drugs.

毫無疑問，這樣的老鼠在使用了麻藥后，比起正常的用了麻藥的老鼠，疼痛感幾乎沒有降低。

Clearly, GABA receptor sites on nerve cells are part of what allows anesthetics to do their job.

顯然位于神經(jīng)細(xì)胞上的GABA接收器是讓麻藥起作用的原因之一。

While the Zurich experiment fills in only one piece of the puzzle, it is an important steptowards learning how these amazing drugs work, and how to make them even better.

盡管蘇黎世大學(xué)做的實(shí)驗(yàn)只解決了一小部分困惑，但是這對(duì)于了解這些神奇的藥物如何工作的，以及怎樣讓它們發(fā)揮更好的效果是重要的一步。