For many years,caffeine's effects have been attributed to 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. To buttress their case that caffeine acts instead by preventing adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives with their ability to dislodge adenosine from its receptors in the rains 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.
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.
(E) challenge the validity of a theory by exposing the inconsistencies and contradictions in it 2. Which of the following, if true, would most weaken the theory proposed by Snyder et al?
(A) At very low concentrations in the human brain, both caffeine and theophylline tend to have depressive rather than stimulatory effects on human behavior.
(B) The ability of caffeine derivatives at very low concentrations to dislodge adenosine from its receptors in mouse brains correlates well with their ability to stimulate mouse locomotion at these low concentrations.
(C) The concentration of cyclic AMP in target neurons in the human brain that leads to increased neuron firing can be produced by several different phosphodiesterase inhibitors in addition to caffeine.
(D) The concentration of caffeine required to dislodge adenosine from its receptors in the human brain is much greater than the concentration that produces behavioral stimulation in humans.
(E) The concentration of IBMX required to dislodge adenosine from its receptors in mouse brains is much smaller than the concentration that stimulates ocomotion in the mouse.
5. The passage suggests that Snyder et al believe that if the older theory concerning caffeine's effects were correct, which of the following would have to be the case?
I. All neurotransmitters would increase the short-term concentration of cyclic AMP in target neurons.
II. Substances other than caffeine that inhibit the production of phosphodiesterase would be stimulants.
III. All concentration levels of caffeine that are high enough to produce stimulation would also inhibit the production of phosphodiesterase.
7. Snyder et al suggest that caffeine's ability to bind to A1 and A2 receptors can be at least partially attributed to which of the following?
9. The last paragraph of the passage performs which of the following functions?
(A) Describes a disconfirming experimental result and reports the explanation given by Snyder et al in an attempt to reconcile this result with their theory.
(B) Specifies the basis for the correlation observed by Snyder et al and presents an explanation in an attempt to make the correlation consistent with the operation of psychoactive drugs other than caffeine.
(C) Elaborates the description of the correlation observed by Snyder et al and suggests an additional explanation in an attempt to make the correlation consistent with the older theory.
(D) Reports inconsistent experimental data and describes the method Snyder et al will use to reanalyze this data.
(E) Provides an example of the hypothesis proposed by Snyder et al and relates this example to caffeine's properties.