Out for the Count
麻醉藥是指能使整個機體或機體局部暫時、可逆性失去知覺及痛覺的藥物。根據(jù)其作用范圍可分為全身麻醉藥及局部麻醉藥,全身麻醉藥及局部麻醉藥根據(jù)其作用特點和給藥方式不同,又可分為吸入麻醉藥和靜脈麻醉藥。直到現(xiàn)在,科學家們依然不能確定這些麻醉藥物如何工作。美國加利福尼亞大學的麻醉學專家詹姆斯·桑尼爾說:“這仍然是神經科學中的一個謎,我們可以使生物體失去知覺,在昏睡中接受手術,然后恢復生物體的意識,但我們卻缺乏充足的證據(jù)說明那些藥物是如何工作的。”
If you've ever had major surgery, you probably remember lying down and waking up--but nothing in between. Learn about anesthetics on this Moment of Science.
If you’ve ever had major surgery, you probably remember lying down and waking up–but nothing in between. Thanks to the anesthesiologist, during the actual surgery you were out of it: immobilized and insensitive to pain. But until recently scientists had little understanding of how anesthetics actually work on the cellular level.
That’s changed thanks to recent experiments performed by researchers at the University of Zurich, in Switzerland. They knew that anesthetics caused pain receptors in the brain to turn off by acting like most drugs do: anesthetizing drugs attach to particular sites on nerve cells and turn them off. The question was, where on nerve cells do these drugs attach?
Nerve cell membranes(細胞膜) have receptors for different kinds of chemicals produced by the brain. Gamma-amino butyric acid(γ-氨基丁酸), or GABA(伽馬氨基丁酸), for example, is a chemical that shuts down nerve cells. The hypothesis was that general anesthesia works by binding to GABA receptors on a nerve cell, thereby activating the receptor and instructing the cell to shut down. So it made sense for the Zurich researchers to focus on GABA receptors.
To do this they worked with mice that had been genetically engineered to have nerve cells with GABA receptors that wouldn’t respond to anesthetics. And sure enough, when such mice were given anesthetic drugs they weren’t nearly as immune to pain as regular mice that had also been given pain-blocking drugs. Clearly, GABA receptor sites on nerve cells are part of what allows anesthetics to do their job.
While the Zurich experiment fills in only one piece of the puzzle, it is an important step towards learning how these amazing drugs work, and how to make them even better.
譯文:
如果你曾經動過手術,你可能會記得躺下和醒來這兩個動作,但是對中間發(fā)生的事情一無所知。多虧了你的麻醉師,在實際的手術過程中你對疼痛全然不知。但直到最近科學家們對麻醉藥如何在細胞水平上發(fā)揮作用仍然了解甚少。
歸功于瑞士蘇黎世大學研究人員的最新研究,這種情況得以改變。他們知道正如許多藥物那樣,麻醉藥讓大腦里的疼痛受體處于關閉狀態(tài)。麻醉藥依附在神經細胞里的特定區(qū)域,并對它們進行麻醉。問題是,這些藥物是依附在神經細胞的的哪個部位呢?
神經細胞膜針對大腦產生的各種化學物質都有受體。如γ-氨基丁酸或伽馬氨基丁酸,都是可以使神經細胞關閉的化學物質。假設全身麻醉與神經細胞上的伽馬氨基丁酸受體有關,那么可以激活受體,指示細胞關閉。因此蘇黎世大學研究人員認為應該著重研究伽馬氨基丁酸受體。
為了此項研究,研究人員們用經過遺傳工程處理后的老鼠做實驗,這些老鼠的伽馬氨基丁酸受體不會對麻醉藥起反應。果然,這些老鼠在注射了麻醉藥后并不像正常的老鼠注射了麻醉藥那樣,對疼痛免疫。顯然,在神經細胞上的伽馬氨基丁酸受體就是麻醉藥發(fā)揮作用的地方。
盡管蘇黎世大學的實驗只解決了謎團中的一小部分,但是研究麻醉藥是怎樣工作的以及怎樣讓它們工作的更好仍是非常重要的。
Notes:
(1)Out for the Count 死的, 毀了的
Count me out for the banana split.
別指望我同你一起分享香蕉味。