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Helplessness and passivity are central themes in describing human depression. Laboratory experiments with animals have uncovered a phenomenon designated “learned helplessness.” Dogs given inescapable shock initially show intense emotionality, but later become passive in the same situation. When the situation is changed from inescapable to escapable shock, the dogs fail to escape even though escape is possible. Neurochemical changes resulting from learned helplessness produce an avoidance escape deficit in laboratory animals.

Is the avoidance deficit caused by prior exposure to inescapable shock learned helplessness or is it simply stress-induced noradrenergic deficiency leading to a deficit in motor activation? Avoidance Escape deficit can be produced in rats by stress alone, i.e., by a brief swim in cold water. But a deficit produced by exposure to extremely traumatic events must be produced by a very different mechanism than the deficit produced by exposure to the less traumatic uncontrollable aversive events in the learned helplessness experiments. A nonaversive parallel to the learned helplessness induced by uncontrollable shock, e.g., induced by uncontrollable food delivery, produces similar results. Moreover, studies have shown the importance of prior experience in learned helplessness. Dogs can be “immunized” against learned helplessness by prior experience with controllable shock. Rats also show a “mastery effect” after extended experience with escapable shock. They work far longer trying to escape from inescapable shock than do rats lacking this prior mastery experience. Conversely, weanling rats given inescapable shock fail to escape shock as adults. These adult rats are also poor to nonaversive discrimination learning.

Certain similarities have been noted between conditions produced in animals by the learned-helplessness procedure and by the experimental neurosis paradigm. In the latter, animals are first trained on a discrimination task and are then tested with discriminative stimuli of increasing similarity. Eventually, as the discrimination becomes very difficult, animals fail to respond and begin displaying abnormal behaviors: first agitation, then lethargy.

It has been suggested that both learned helplessness and experimental neurosis involve inhibition of motivation centers and pathways by limbic forebrain inhibitory centers, especially in the septal area. The main function of this inhibition is compensatory, providing relief from anxiety or distress. In rats subjected to the learned-helplessness and experimental-neurosis paradigms, stimulation of the septum produces behavioral arrest, lack of behavioral initiation and lethargy, while rats with septal lesions do not show learned helplessness.

How analogous the model of learned helplessness and the paradigm of stress induced neurosis are to human depression is not entirely clear. Inescapable noise or unsolvable problems have been shown to result in conditions in humans similar to those induced in laboratory animals, but an adequate model of human depression must also be able to account for the cognitive complexity of human depression.

1. The primary purpose of the passage is to
(A) propose a cure for depression in human beings
(B) discuss research possibly relevant to depression in human beings
(C) criticize the result of experiments which induce depression in laboratory animals
(D) raise some questions about the propriety of using laboratory animals for research
(E) suggest some ways in which depression in animals differs from depression in humans

2. The author raises the question at the beginning of the second paragraph in order to
(A) prove that learned helplessness is caused by neurochemical changes
(B) demonstrate that learned helplessness is also caused by nonaversive discrimination learning
(C) suggest that further research is needed to determine the exact causes of learned helplessness
(D) refute a possible objection based on an alternative explanation of the cause of learned helplessness
(E) express doubts about the structure of the experiments that created learned helplessness in dogs

3. It can be inferred from the passage that rats with septal lesions do not show learned helplessness because
(A) such rats were immunized against learned helplessness by prior training
(B) the lesions blocked communication between the limbic forebrain inhibitory centers and motivation centers
(C) the lesions prevented the rats from understanding the inescapability of the helplessness situation
(D) a lack of stimulation of the septal area does not necessarily result in excited behavior
(E) lethargy and other behavior associated with learned helplessness can be induced by the neurosis paradigm

4. It can be inferred that the most important difference between experiments inducing learned helplessness by inescapable shock and the nonaversive parallel mention edin is that the nonaversive parallel
(A) did not use pain as a stimuli to be avoided
(B) failed to induce learned helplessness in subject animals
(C) reduced the extent of learned helplessness
(D) caused a more traumatic reaction in the animals
(E) used only rats rather than dogs as subjects

5. The author cites the “mastery effect” primarily in order to
(A) prove the avoidance deficit caused by exposure to inescapable shock is not caused by shock per se but by the inescapability
(B) cast doubts on the validity of models of animal depression when applied to depression in human beings
(C) explain the neurochemical changes in the brain that cause learned helplessness
(D) suggest that the experimental neurosis paradigm and the learned helplessness procedure produce similar behavior in animals
(E) argue that learned helplessness is simply a stress-induced noradrenergic deficiency

6. Which of the following would be the most logical continuation of the passage?
(A) An explanation of the connection between the septum and the motivation centers of the brains of rats
(B) An examination of techniques used to cure animals of learned helplessness
(C) A review of experiments designed to create stress-induced noradrenergic deficiencies in humans
(D) A proposal for an experiment to produce learned helplessness and experimental neurosis in humans
(E) An elaboration of the differences between human depression and similar animal behavior