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Directions: Read the Passage carefully and answer the question as follow.
Caffeine, the stimulant in coffee, has been called 
“the most widely used psychoactive substance on Earth .”
Synder, Daly and Bruns have recently proposed that 
caffeine affects behavior by countering the activity in 
(5) 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.
(10) 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 propose that caffeine, which is struc-
(15)  turally 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.For many years, caffeine’s effects have been attri-
(20)  buted to its inhibition of the production of phosphodi-
esterase, an enzyme that breaks down the chemical 
called cyclic AMP.A number of neurotransmitters exert 
their effects by first increasing cyclic AMP concentra-
tions in target neurons. Therefore, prolonged periods at 
(25)  the elevated concentrations, as might be brought about 
by a phosphodiesterase inhibitor, could lead to a greater 
amount of neuron firing and, consequently, to behav-
ioral stimulation. But Snyder et al point out that the 
caffeine concentrations needed to inhibit the production 
(30)  of phosphodiesterase in the brain are much higher than 
those that produce stimulation. Moreover, other com-
pounds that block phosphodiesterase’s activity are not 
stimulants.
To buttress their case that caffeine acts instead by pre-
(35)  venting 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 
(40) 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 locomo-
tion.” Theophylline, a close structural relative of caffeine 
and the major stimulant in tea, was one of the most 
(45) 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-isobuty1-1-methylxanthine(IBMX), which bound very 
(50) well but actually depressed mouse locomotion. Snyder 
et al suggest that this is not a major stumbling block 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 
(55) known only for its stimulatory effects, displays this 
 property, depressing mouse locomotion at very low  
 concentrations and stimulating it at higher ones.
Q. 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?
(a) The chemical relationship between caffeine and phosphodiesterase 
(b) The structural relationship between caffeine and adenosine 
(c) The structural similarity between caffeine and neurotransmitters 
(d) The ability of caffeine to stimulate behavior 
(e) The natural occurrence of caffeine and adenosine in the brain
  • a)
    The chemical relationship between caffeine and phosphodiesterase 
  • b)
    The structural relationship between caffeine and adenosine 
  • c)
    The structural similarity between caffeine and neurotransmitters 
  • d)
    The ability of caffeine to stimulate behavior 
  • e)
    The natural occurrence of caffeine and adenosine in the brain
Correct answer is option 'B'. Can you explain this answer?
Most Upvoted Answer
Directions: Read the Passage carefully and answer the question as foll...
B is the best answer.
This question asks you to identify information that is suggested rather than directly stated in the passage. To answer it, first look for the location in the passage of the information specified in the question. The A1 and A2 receptors are mentioned in lines 23-26. Lines 27-35 go on to describe Snyder et al’s hypothesis about the effects of caffeine on behavior. They propose that caffeine, “which is structurally similar to adenosine,” is able to bind to A1 and A2 receptors in the brain, the same receptors that adenosine normally binds to. Thus, the passage suggests that the structural relationship between caffeine and adenosine may be partially responsible for caffeine’s ability to bind to A1 and A2 receptors.
Free Test
Community Answer
Directions: Read the Passage carefully and answer the question as foll...
B is the best answer.
This question asks you to identify information that is suggested rather than directly stated in the passage. To answer it, first look for the location in the passage of the information specified in the question. The A1 and A2 receptors are mentioned in lines 23-26. Lines 27-35 go on to describe Snyder et al’s hypothesis about the effects of caffeine on behavior. They propose that caffeine, “which is structurally similar to adenosine,” is able to bind to A1 and A2 receptors in the brain, the same receptors that adenosine normally binds to. Thus, the passage suggests that the structural relationship between caffeine and adenosine may be partially responsible for caffeine’s ability to bind to A1 and A2 receptors.
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Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.According to Snyder et al, all of the following compounds can bind to specific receptors in the brain EXCEPT

Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.According so Snyder et al, caffeine differs from adenosine in that caffeine

Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.The primary purpose of the passage is to

Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.The author quotes Snyder et al in lines 38-43 most probably in order to

Over the past 20,000 years, the average volume of the human male brain has decreased from 1,500 cubic centimeters to 1,350 cc, losing a chunk the size of a tennis ball. The female brain has shrunk by about the same proportion. If our brain keeps dwindling at this rate over the next 20,000 years, it will start to approach the size of the brain found in Homo erectus, a relative that lived half a million years ago and had a brain volume of only 1,100 cc.Some believe the erosion of our gray matter means that modern humans are indeed getting dumber. A common measure of intelligence - the encephalization quotient or EQ, defined as the ratio of brain volume to body mass - has been found to be decreasing in the recent past. Recent studies of human fossils suggest the brain shrank more quickly than the body in near-modern times. More importantly, analysis of the genome casts doubt on the notion that modern humans are simply daintier but otherwise identical versions of our ancestors, right down to how we think and feel. Another study concluded that our present EQ is the same as that of the Cro-Magnons - our ancestors who lived 30,000 years ago in Europe and were known more for brawniness rather than brilliance.On the other hand, other anthropologists such as Hawks believe that as the brain shrank, its wiring became more efficient, transforming us into quicker, more agile thinkers. They explain the shrinking by arguing that over the very period that the brain shrank, our DNA accumulated numerous adaptive mutations related to brain development and neurotransmitter systemsan indication that even as the organ got smaller, its inner workings changed.This explanation may be plausible, considering that the brain is such a glutton for fuel that it globs up to 20% of all the calories. To optimize this, the evolution may be moving towards a more efficient smaller brain that yields the most intelligence for the least energy. A boom in the human population in the last 20,000 years ago greatly improved the odds of such a fortuitous development since the more the individuals, the bigger the gene pool, and the greater the chance for an unusual advantageous mutation to happen.The man-made product that is closest to the brain, the microprocessor, has seen similar evolution. A microprocessor consists of transistors- the human equivalent of neuron that participates in decision making connected with wires that act as messengers between neurons. The first microprocessors had extremely simple architectures and were not optimized for a certain set of tasks but were more general purpose. Consequently, a lot of the power they consumed was dissipated in internal wiring and not in decision making. With refinements, the architectures became more and more attuned to the tasks that the microprocessor most commonly needed to do. Consequently, for the same number of transistors the amount of wiring decreased by a factor of 3 while the microprocessors processing speed increased by a factor of 10. While active research is still to conclude whether the same holds true in case of the brain, one can only hope that the results are along the lines of the microprocessor.Which of the following if true would weaken the assertion that humans are getting dumber with the erosion of brain volume?

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Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.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?(a) The chemical relationship between caffeine and phosphodiesterase(b) The structural relationship between caffeine and adenosine(c) The structural similarity between caffeine and neurotransmitters(d) The ability of caffeine to stimulate behavior(e) The natural occurrence of caffeine and adenosine in the braina)The chemical relationship between caffeine and phosphodiesteraseb)The structural relationship between caffeine and adenosinec)The structural similarity between caffeine and neurotransmittersd)The ability of caffeine to stimulate behaviore)The natural occurrence of caffeine and adenosine in the brainCorrect answer is option 'B'. Can you explain this answer?
Question Description
Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.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?(a) The chemical relationship between caffeine and phosphodiesterase(b) The structural relationship between caffeine and adenosine(c) The structural similarity between caffeine and neurotransmitters(d) The ability of caffeine to stimulate behavior(e) The natural occurrence of caffeine and adenosine in the braina)The chemical relationship between caffeine and phosphodiesteraseb)The structural relationship between caffeine and adenosinec)The structural similarity between caffeine and neurotransmittersd)The ability of caffeine to stimulate behaviore)The natural occurrence of caffeine and adenosine in the brainCorrect answer is option 'B'. Can you explain this answer? for GMAT 2024 is part of GMAT preparation. The Question and answers have been prepared according to the GMAT exam syllabus. Information about Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.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?(a) The chemical relationship between caffeine and phosphodiesterase(b) The structural relationship between caffeine and adenosine(c) The structural similarity between caffeine and neurotransmitters(d) The ability of caffeine to stimulate behavior(e) The natural occurrence of caffeine and adenosine in the braina)The chemical relationship between caffeine and phosphodiesteraseb)The structural relationship between caffeine and adenosinec)The structural similarity between caffeine and neurotransmittersd)The ability of caffeine to stimulate behaviore)The natural occurrence of caffeine and adenosine in the brainCorrect answer is option 'B'. Can you explain this answer? covers all topics & solutions for GMAT 2024 Exam. Find important definitions, questions, meanings, examples, exercises and tests below for Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.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?(a) The chemical relationship between caffeine and phosphodiesterase(b) The structural relationship between caffeine and adenosine(c) The structural similarity between caffeine and neurotransmitters(d) The ability of caffeine to stimulate behavior(e) The natural occurrence of caffeine and adenosine in the braina)The chemical relationship between caffeine and phosphodiesteraseb)The structural relationship between caffeine and adenosinec)The structural similarity between caffeine and neurotransmittersd)The ability of caffeine to stimulate behaviore)The natural occurrence of caffeine and adenosine in the brainCorrect answer is option 'B'. Can you explain this answer?.
Solutions for Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.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?(a) The chemical relationship between caffeine and phosphodiesterase(b) The structural relationship between caffeine and adenosine(c) The structural similarity between caffeine and neurotransmitters(d) The ability of caffeine to stimulate behavior(e) The natural occurrence of caffeine and adenosine in the braina)The chemical relationship between caffeine and phosphodiesteraseb)The structural relationship between caffeine and adenosinec)The structural similarity between caffeine and neurotransmittersd)The ability of caffeine to stimulate behaviore)The natural occurrence of caffeine and adenosine in the brainCorrect answer is option 'B'. Can you explain this answer? in English & in Hindi are available as part of our courses for GMAT. Download more important topics, notes, lectures and mock test series for GMAT Exam by signing up for free.
Here you can find the meaning of Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.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?(a) The chemical relationship between caffeine and phosphodiesterase(b) The structural relationship between caffeine and adenosine(c) The structural similarity between caffeine and neurotransmitters(d) The ability of caffeine to stimulate behavior(e) The natural occurrence of caffeine and adenosine in the braina)The chemical relationship between caffeine and phosphodiesteraseb)The structural relationship between caffeine and adenosinec)The structural similarity between caffeine and neurotransmittersd)The ability of caffeine to stimulate behaviore)The natural occurrence of caffeine and adenosine in the brainCorrect answer is option 'B'. Can you explain this answer? defined & explained in the simplest way possible. Besides giving the explanation of Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.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?(a) The chemical relationship between caffeine and phosphodiesterase(b) The structural relationship between caffeine and adenosine(c) The structural similarity between caffeine and neurotransmitters(d) The ability of caffeine to stimulate behavior(e) The natural occurrence of caffeine and adenosine in the braina)The chemical relationship between caffeine and phosphodiesteraseb)The structural relationship between caffeine and adenosinec)The structural similarity between caffeine and neurotransmittersd)The ability of caffeine to stimulate behaviore)The natural occurrence of caffeine and adenosine in the brainCorrect answer is option 'B'. Can you explain this answer?, a detailed solution for Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.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?(a) The chemical relationship between caffeine and phosphodiesterase(b) The structural relationship between caffeine and adenosine(c) The structural similarity between caffeine and neurotransmitters(d) The ability of caffeine to stimulate behavior(e) The natural occurrence of caffeine and adenosine in the braina)The chemical relationship between caffeine and phosphodiesteraseb)The structural relationship between caffeine and adenosinec)The structural similarity between caffeine and neurotransmittersd)The ability of caffeine to stimulate behaviore)The natural occurrence of caffeine and adenosine in the brainCorrect answer is option 'B'. Can you explain this answer? has been provided alongside types of Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.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?(a) The chemical relationship between caffeine and phosphodiesterase(b) The structural relationship between caffeine and adenosine(c) The structural similarity between caffeine and neurotransmitters(d) The ability of caffeine to stimulate behavior(e) The natural occurrence of caffeine and adenosine in the braina)The chemical relationship between caffeine and phosphodiesteraseb)The structural relationship between caffeine and adenosinec)The structural similarity between caffeine and neurotransmittersd)The ability of caffeine to stimulate behaviore)The natural occurrence of caffeine and adenosine in the brainCorrect answer is option 'B'. Can you explain this answer? theory, EduRev gives you an ample number of questions to practice Directions: Read the Passage carefully and answer the question as follow.Caffeine, the stimulant in coffee, has been called“the most widely used psychoactive substance on Earth .”Synder, Daly and Bruns have recently proposed thatcaffeine affects behavior by countering the activity in(5) the human brain of a naturally occurring chemical calledadenosine. Adenosine normally depresses neuron firingin many areas of the brain. It apparently does this byinhibiting the release of neurotransmitters, chemicalsthat carry nerve impulses from one neuron to the next.(10) Like many other agents that affect neuron firing,adenosine must first bind to specific receptors onneuronal membranes. There are at least two classesof these receptors, which have been designated A1 andA2. Snyder et al propose that caffeine, which is struc-(15) turally similar to adenosine, is able to bind to both typesof receptors, which prevents adenosine from attachingthere and allows the neurons to fire more readily thanthey otherwise would.For many years, caffeine’s effects have been attri-(20) buted to its inhibition of the production of phosphodi-esterase, an enzyme that breaks down the chemicalcalled cyclic AMP.A number of neurotransmitters exerttheir effects by first increasing cyclic AMP concentra-tions in target neurons. Therefore, prolonged periods at(25) the elevated concentrations, as might be brought aboutby a phosphodiesterase inhibitor, could lead to a greateramount of neuron firing and, consequently, to behav-ioral stimulation. But Snyder et al point out that thecaffeine concentrations needed to inhibit the production(30) of phosphodiesterase in the brain are much higher thanthose that produce stimulation. Moreover, other com-pounds that block phosphodiesterase’s activity are notstimulants.To buttress their case that caffeine acts instead by pre-(35) venting adenosine binding, Snyder et al compared thestimulatory effects of a series of caffeine derivatives withtheir ability to dislodge adenosine from its receptors inthe brains of mice. “In general,” they reported, “theability of the compounds to compete at the receptors(40) correlates with their ability to stimulate locomotion inthe mouse; i.e., the higher their capacity to bind at thereceptors, the higher their ability to stimulate locomo-tion.” Theophylline, a close structural relative of caffeineand the major stimulant in tea, was one of the most(45) effective compounds in both regards.There were some apparent exceptions to the generalcorrelation observed between adenosine-receptor bindingand stimulation. One of these was a compound called3-isobuty1-1-methylxanthine(IBMX), which bound very(50) well but actually depressed mouse locomotion. Snyderet al suggest that this is not a major stumbling block totheir hypothesis. The problem is that the compound hasmixed effects in the brain, a not unusual occurrence withpsychoactive drugs. Even caffeine, which is generally(55) known only for its stimulatory effects, displays thisproperty, depressing mouse locomotion at very low concentrations and stimulating it at higher ones.Q.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?(a) The chemical relationship between caffeine and phosphodiesterase(b) The structural relationship between caffeine and adenosine(c) The structural similarity between caffeine and neurotransmitters(d) The ability of caffeine to stimulate behavior(e) The natural occurrence of caffeine and adenosine in the braina)The chemical relationship between caffeine and phosphodiesteraseb)The structural relationship between caffeine and adenosinec)The structural similarity between caffeine and neurotransmittersd)The ability of caffeine to stimulate behaviore)The natural occurrence of caffeine and adenosine in the brainCorrect answer is option 'B'. Can you explain this answer? tests, examples and also practice GMAT tests.
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