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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. According so Snyder et al, caffeine differs from   adenosine in that caffeine
  • a)
    stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans only 
  • b)
    has mixed effects in the brain, whereas adenosine has only a stimulatory effect 
  • c)
    increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrations
  • d)
    permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such release 
  • e)
    inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firing
Correct answer is option 'D'. Can you explain this answer?
Verified Answer
Directions: Read the Passage carefully and answer the question as foll...
D is the best answer.
Lines 11-23 state that adenosine “depresses neuron firing” by binding to specific receptors on neuronal membranes, which in turn inhibits the release of neurotransmitters. Lines 27-35 describe Snyder et al’s hypothesis about caffeine. They propose that caffeine binds to specific receptors on neuronal membranes, which prevents adenosine from binding to those receptors and “allows the neurons to fire more readily that they otherwise would”. Therefore, according to Snyder et al, caffeine differs from adenosine in that caffeine permits neurotransmitter release when it is bound to adenosine receptors, whereas adenosine inhibits neruotransmitter release.
View all questions of this test
Most Upvoted Answer
Directions: Read the Passage carefully and answer the question as foll...
D is the best answer.
Lines 11-23 state that adenosine “depresses neuron firing” by binding to specific receptors on neuronal membranes, which in turn inhibits the release of neurotransmitters. Lines 27-35 describe Snyder et al’s hypothesis about caffeine. They propose that caffeine binds to specific receptors on neuronal membranes, which prevents adenosine from binding to those receptors and “allows the neurons to fire more readily that they otherwise would”. Therefore, according to Snyder et al, caffeine differs from adenosine in that caffeine permits neurotransmitter release when it is bound to adenosine receptors, whereas adenosine inhibits neruotransmitter release.
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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.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?(

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

Scientific advances in the latter half of the twentieth century have allowed researchers to study the chemical activities taking place in the human brain during the sleep cycle in more detail. In the 1970s, Jacobs employed these advances to postulate that dreams and hallucinations share a common neurochemical mechanism with respect to the neurotransmitters serotonin and norepinephrine that accounts for the observable similarities between the two states of mind. To test the theory, researchers attempted to elucidate the role of these transmitters in the normal sleep cycle and the effect of hallucinogenic drugs on them.Although scientists still have much to discover about the chemical complexities of the brain, serotonin appears important for managing sleep, mood, and appetite, among other important functions, while neurons release norepinephrine to facilitate alertness and mental focus.Both are discharged in high quantities only during waking states. At the onset of sleep, the activity levels of neurons that release both the neurotransmitters drop, allowing the brain first to enter the four non-rapid eye movement (Non-REM) stages of sleep. When the brain is ready to enter the fifth stage, REM, which is associated with dreaming, the levels of these two chemicals drop virtually to zero. The Jacobs hypothesis held that the absence of norepinephrine was required to enable the brain to remain asleep, while the absence of serotonin was necessary to allow dreaming to occur.Lysergic acid diethylamide, or LSD, is a semi-synthetic psychedelic drug which causes significant alteration of the senses, memories and awareness; at doses higher than 20 micrograms, it can have a hallucinogenic effect.LSD mimics serotonin well enough to be able to bind at most of the neurotransmitter’s receptor sites, largely inhibiting normal transmission. In addition, the drug causes the locus ceruleus, a cluster of neurons containing norepinephrine, to greatly accelerate activity. If the drug stimulates norepinephrine, thereby precluding sleep, and inhibits serotonin, which Jacobs had postulated was a necessary condition for dreaming, then the resulting hallucinations could merely be “dreaming while awake.” The research thus far is promising but inconclusive; future scientific advances should allow this theory to be tested more rigorously.Q.Which of the following best represents the author’s primary goal in writing the passage?

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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 so Snyder et al, caffeine differs from adenosine in that caffeinea)stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans onlyb)has mixed effects in the brain, whereas adenosine has only a stimulatory effectc)increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrationsd)permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such releasee)inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firingCorrect answer is option 'D'. 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.According so Snyder et al, caffeine differs from adenosine in that caffeinea)stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans onlyb)has mixed effects in the brain, whereas adenosine has only a stimulatory effectc)increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrationsd)permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such releasee)inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firingCorrect answer is option 'D'. 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.According so Snyder et al, caffeine differs from adenosine in that caffeinea)stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans onlyb)has mixed effects in the brain, whereas adenosine has only a stimulatory effectc)increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrationsd)permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such releasee)inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firingCorrect answer is option 'D'. 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.According so Snyder et al, caffeine differs from adenosine in that caffeinea)stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans onlyb)has mixed effects in the brain, whereas adenosine has only a stimulatory effectc)increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrationsd)permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such releasee)inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firingCorrect answer is option 'D'. 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.According so Snyder et al, caffeine differs from adenosine in that caffeinea)stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans onlyb)has mixed effects in the brain, whereas adenosine has only a stimulatory effectc)increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrationsd)permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such releasee)inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firingCorrect answer is option 'D'. 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.According so Snyder et al, caffeine differs from adenosine in that caffeinea)stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans onlyb)has mixed effects in the brain, whereas adenosine has only a stimulatory effectc)increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrationsd)permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such releasee)inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firingCorrect answer is option 'D'. 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.According so Snyder et al, caffeine differs from adenosine in that caffeinea)stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans onlyb)has mixed effects in the brain, whereas adenosine has only a stimulatory effectc)increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrationsd)permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such releasee)inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firingCorrect answer is option 'D'. 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.According so Snyder et al, caffeine differs from adenosine in that caffeinea)stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans onlyb)has mixed effects in the brain, whereas adenosine has only a stimulatory effectc)increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrationsd)permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such releasee)inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firingCorrect answer is option 'D'. 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.According so Snyder et al, caffeine differs from adenosine in that caffeinea)stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans onlyb)has mixed effects in the brain, whereas adenosine has only a stimulatory effectc)increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrationsd)permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such releasee)inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firingCorrect answer is option 'D'. 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.According so Snyder et al, caffeine differs from adenosine in that caffeinea)stimulates behavior in the mouse and in humans, whereas adenosine stimulates behavior in humans onlyb)has mixed effects in the brain, whereas adenosine has only a stimulatory effectc)increases cyclic AMP concentrations in target neurons, whereas adenosine decreases such concentrationsd)permits release of neurotransmitters when it is bound to adenosine receptors, whereas adenosine inhibits such releasee)inhibits both neuron firing and the production of phosphodiesterase when there is a sufficient concentration in the brain, whereas adenosine inhibits only neuron firingCorrect answer is option 'D'. Can you explain this answer? tests, examples and also practice GMAT tests.
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