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我的一点愚见：对大全10的第二题的分析请见蓝色字 Caffeine, the stimulant in coffee, has been called “the most widely used psychoactive substance on Earth.” Snyder, Daly and Bruns have recently proposed
that caffeine affect behavior by countering the activity in the human brain of a naturally occurring chemical called adenosine. Adenosine normally depresses neuron firing in many areas of the brain. It apparently does this by inhibiting the release of neurotransmitters, chemicals that carry nerve impulses from one neuron to the next. Like many other agents that affect neuron firing, adenosine must first bind to specific receptors on neuronal membranes. There are at least two classes of these receptors, which have been designated A1 and A2. Snyder et al (et al: abbr. (Lat) 以及其他人，等人) propose that caffeine, which is structurally similar to adenosine, is able to bind to both types of receptors, which prevents adenosine from attaching there and allows the neurons to fire more readily than they otherwise would.[新观点：Caffeine通过抵制Adenosine来起到刺激作用àAdenosine是如何作用的：通过和receptors结合抑止兴奋àCaffeine是如何抵制Adenosine作用的：由于结构相似，caffeine通过和receptors结合阻碍adenosine和receptors结合，从而起到刺激作用] For many years, caffeine’s effects have been attributed to [前果后因] its inhibition of the production of phosphodiesterase, an enzyme that breaks down the chemical called cyclic AMP. A number of neurotransmitters exert their effects by first increasing cyclic AMP concentrations in target neurons. Therefore, prolonged periods at the elevated concentrations, as might be brought about by a phosphodiesterase inhibitor, could lead to a greater amount of neuron firing and, consequently, to behavioral stimulation. But
Snyder et al point out that the caffeine concentrations needed to inhibit the production of phosphodiesterase in the brain are much higher than those that produce stimulation. Moreover, other compounds that block phosphodiesterase’s activity are not stimulants. [老观点Caffeine是如何作用的à批驳老观点：用于抑止ph产生的caffeine浓度大大高于产生刺激作用所需的caffeine的浓度。换而言之，在caffeine的浓度还没有达到抑止ph产生的浓度时，刺激作用已经产生了。] To buttress their case that caffeine acts instead by preventing adenosine binding, Snyder et al compared the stimulatory effects of a series of caffeine derivatives with their ability to dislodge adenosine from its receptors in the brains of mice.
“In general,” they reported, “the ability of the compounds to compete at the receptors correlates with their ability to stimulate locomotion in the mouse; i.e., the higher their capacity to bind at the receptors, the higher their ability to stimulate locomotion.”
Theophylline, a close structural relative of caffeine and the major stimulant in tea, was one of the most effective compounds in both regards. [新观点的理论依据：compounds与receptors结合的能力越高，产生刺激作用的能力就越高。如果想削弱这一新观点，可以说：用于阻止ad和receptors结合的caffeine的浓度高于产生刺激作用的caffeine的浓度。即caffeine的浓度在还没有达到阻止ad和receptors结合的时候就已经可以产生刺激作用了，所以Synder他们的把“compounds与receptors结合的能力”作为caffeine刺激作用的前提条件就是不充分的了。] There were some apparent exceptions to the general correlation observed between adenosine-receptor binding and stimulation. One of these was a compound called 3-isobutyl-1-methylxanthine (IBMX), which bound very well but actually depressed mouse locomotion. Snyder et al suggests that this is not a major stumbling block (stumbling block: n.障碍物, 绊脚石) to their hypothesis. The problem is that the compound has mixed effects in the brain, a not unusual occurrence with psychoactive drugs.
Even caffeine, which is generally known only for its stimulatory effects, displays this property, depressing mouse locomotion at very low concentrations and stimulating it at higher ones. [延伸性内容] | 
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发表于 2007-1-14 16:08:00
