Much of the research on hallucinogenic drugs such
as LSD has focused on the neurotransmitter serotonin,
a chemical that when released from a presynaptic
serotonin-secreting neuron causes the transmission of
(5) a nerve impulse across a synapse to an adjacent
postsynaptic, or target, neuron. There are two major
reasons for this emphasis. First, it was discovered
early on that many of the major hallucinogens have a
molecular structure similar to that of serotonin. In
(10) addition, animal studies of brain neurochemistry
following administration of hallucinogens invariably
reported changes in serotonin levels.
Early investigators correctly reasoned that the
structural similarity to the serotonin molecule might
(15) imply that LSD’s effects are brought about by an
action on the neurotransmission of serotonin in the
brain. Unfortunately, the level of technical expertise
in the field of brain research was such that this
hypothesis had to be tested on peripheral tissue
(20) (tissue outside the brain). Two different groups of
scientists reported that LSD powerfully blockaded
serotonin’s action. Their conclusions were quickly
challenged, however. We now know that the action
of a drug at one site in the body does not necessarily
(25) correspond to the drug’s action at another site,
especially when one site is in the brain and the other
is not.
By the 1960’s, technical advances permitted the
direct testing of the hypothesis that LSD and related
(30) hallucinogens act by directly suppressing the activity
of serotonin-secreting neurons themselves—the so-
called presynaptic hypothesis. Researchers reasoned
that if the hllucinogenic drugs act by suppressing the
activity of serotonin-secreting neurons, then drugs
(35) administered after these neurons had been destroyed
should have no effect on behavior, because the
system would already be maximally suppressed.
Contrary to their expectations, neuron destruction
enhanced the effect of LSD and related hallucinogens
(40) on behavior. Thus, hallucinogenic drugs apparently
do not act directly on serotonin-secreting neurons.
However, these and other available data do support
an alternative hypothesis, that LSD and related drugs
act directly at receptor sites on serotonin target
(45) neurons (the postsynaptic hypothesis). The fact that
LSD elicits “serotonin syndrome” —that is, causes
the same kinds of behaviors as does the adminis-
tration of serotonin—in animals whose brains are
depleted of serotonin indicates that LSD acts directly
(50)on serotonin receptors, rather than indirectly through
the release of stores of serotonin. The enhanced effect
of LSD reported after serotonin depletion could be
due to a proliferation of serotonin receptor sites on
serotonin target neurons. This phenomenon often
(55) follows neuron destruction or neurotransmitter
depletion; the increase in the number of receptor sites
appears to be a compensatory response to decreased
input. Significantly, this hypothesis is supported by
data from a number of different laboratories.
23. The author’s attitude toward early researchers’
reasoning concerning the implications of
similarities in the structures of serotonin and
LSD molecules can best be described as one of
(A) complete agreeement
(B) reluctant support
(C) subtle condescension
(D) irreverent dismissal
(E) strong opposition
答案是B,
我有很大疑惑
文章最后结论是LSD是对 serotonin 的receptor直接作用,而非line13所说的reason出的对neurotransmission of serotonin 发生作用。明显此implicaton是错的,但词句用了correctly。那么作者的真正态度又是什么呢?既然错了,为什么还说正确的推理出了。。。。
关键句:
Early investigators correctly reasoned that the
structural similarity to the serotonin molecule might
(15) imply that LSD’s effects are brought about by an
action on the neurotransmission of serotonin in the
brain.
其次分子结构的相同的若是我猜测的话有两种可能
1,对receptor有类似作用(此为文章最后结论)
2,无作用,干扰了原物质的正常传递等过程(此为上面所列关键句的错误结论)
最后reluctant support 到底是什么含义呢?