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Part II: Learned helplessness
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MARTIN E. P. SELIGMAN and JAY M. WEISS
PART
II:
LEARNED
HELPLESSNESS
MARTIN E. P. SELIGMANand AIDAN ALTENOR* The focus of this presentation will be restricted to a fairly rigorous examination of the data bearing on the three competing theories which have emerged to account for the debilitating effects of prior exposure to inescapable shocks in dogs and rats. The three theories are: (a) learned helplessness (Maier, Seligman and Solomon. 1969 ; Seligman, Maier and Solomon, 1971; Seligman, 1975; Maier and Seligman, 1976); (b) a norepinephrine (NE) depletion hypothesis proposed to account for the interference effects evidenced following exposure to inescapable shocks only in the dog (Weiss, Glazer and Pohorecky, 1976); (c) a learned inactivity hypothesis to account for the deficits evidenced following exposure to inescapable shock only in the rat (Glazer and Weiss, 1976a, b). In this presentation, we will argue (1) that the dog data are explained better by learned helplessness than by the NE depletion view, since five sets of findings, ignored and unaccounted for by the NE depletion view, are accounted for by learned helplessness, whereas all dog data explained by NE depletion are also explained by learned helplessness; and (2) that the rat data are better explained by learned helplessness than learned inactivity, since 10 sets of findings, ignored and unaccounted for by learned inactivity, are accounted for by learned helplessness, whereas all rat data explained by learned inactivity are also explained by learned helplessness. In our response to Professor Weiss’ presentation, we shall argue (3) that Weiss has collected data which are explained by NE depletion and not by learned helplessness, but they are data about the effects of stress per se, not uncontrollable stress; and that (4) Professor Weiss’ learned inactivity data are equally well explained by learned helplessness. Definition of ,hypotheses
The learned helplessness hypothesis (Maier, Seligman and Solomon, 1969; Seligman, Maier and Solomon, 1971; Maier and Seligman, 1976) asserts that during exposure to an uncontrollable outcome, the animal learns of the lack of contingency between its responses and the outcome. That is, it learns that it has no control over the outcome. Such learning produces three deficits. One of these deficits is motivational: dogs and rats which have been exposed to inescapable shocks have a reduced tendency to initiate subsequent escape responding in the presence of shock because part of the incentive for making such responses is the expectation that they will bring relief. If the animal has previously learned that its responses have no effect on relief, this contravenes the expectation. Thus the organism’s motivation to respond is undermined by experience with lack of control. Note that the motivational deficit of the learned helplessness hypothesis has built into it an inactivity notion-the foundation of the learned inactivity hypothesis. There are, in addition, two other effects not postulated by the learned inactivity hypothesis. There is a cognitive deficit: exposure to uncontrollable events interferes with the animal’s ability to learn about contingent relationships between its future behavior and outcomes. In general, if we have acquired a cognitive set in which As are irrelevant to Bs, it will be more difficult to learn that As produce Bs when they do. And, there is an emotional deficit: exposure to uncontrollable events produces greater emotional disruption than exposure to controllable events, first anxiety, then depression. The NE depletion hypothesis which Weiss (Weiss, Glazer and Pohorecky, 1976) has proposed to explain the interference effects in our dogs, and nor in our rats, asserts that * Martin Seligman originally delivered these remarks in live debate with Jay Weiss. Aidan Altenor had a major role in the thinking which went into the debate and into the revision of the transcripts into final written form. Preparation of this paper was supported by a National Institute of Mental Health Grant (MH-19604) to Martin E. P. Se&man and a National Institute of Mental Health Postdoctoral Fellowship (MH-07682) to Aidan Altenor. Martin E. P. Seligman was a fellow at the Center for Advanced Studies in the Behavioral Sciences. Stanford. California. during part of the preparation of this paper.
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inescapable shock produces severe deficiency in central noradrenergic activity. A low norepinephrine level will allow for only a limited amount of motor activity. Following inescapable shock, the activity allowed for by the noradrenergic deficits is insufficient for learning and performing the correct response in shuttle avoidance. Since escapable shock does not produce noradrenergic deficiency, sufficient motor activity can occur for adequate performance on escape and avoidance. The major finding which led Weiss and his colleagues to see a need to postulate NE depletion in dogs was that following one session of inescapable shock, shock-escapeavoidance learning was normal 48 h later (Overmier and Seligman, 1967). Miller and Weiss (1969) originally argued that things that are learned do not disappear in 48 h. Further, there is evidence that a noradrenergic process is involved in the mediation of overt behavior (cf. Herman, 1970), that noradrenergic activity is disrupted by exposure to inescapable shock (Maynert and Levi, 1964), and that the noradrenergic disruption recovers following exposure to inescapable shock (Maynert and Levi, 1964). Hence, exposure to inescapable shock produces a depletion of norepinephrine, which causes motoric inactivation. The resultant NE deficit is transient and the transient effect ob~ined in dogs can be so explained. It should be mentioned that the data summoned by Weiss to explain interference in dogs are obtained from rats. There are no published data examining the time course of NE depletion caused by inescapable shock in the dog. A learned inactivity hypothesis has been generated by Glazer and Weiss (1976a, b) [and, more recently, Anisman, de Catanzaro and Remington (19781-Jto account for the interference effects produced by inescapable shock in the rat. According to this hypothesis, exposure to inescapable shock, particularly long duration shock (5 s or more), results in inactivity in the rat. This is because the rat becomes still during a long shock, and this inactivity is adventitiously paired with shock termination. Weiss and Glazer noted that during long duration shock, there is, early in training, an initial burst of activity with shock onset. This activity declines with continued exposure to shock on a given trial. During repeated exposure to the long duration shock, the rat tends to become inactive much sooner after shock onset, suggesting that the rat learns through adventitious reinforcement to become passive or inactive. This hypothesis suggests that shocks of less than 5 s will not produce interference with subsequent learning to escape shock. It also suggests that if two groups of rats are matched for activity or inactivity, there should be no difference in their subsequent escape learning. Tog evidence unexplained by the NE depletion hypothesis The piece of data from the literature in dogs which Jay Weiss takes as supportive of the NE depletion hypothesis is the finding regarding changes in learned helplessness effects over time. Overmier and Seligman {1967) demonstrated that a single exposure to inescapable shock produced extreme interference or helplessness in 2/3 of the dogs after a 24 h delay. However, after 48 h delay there was only minimal interference after shock exposure. When the animals were tested 72 h later, the effects of learned helplessness had wholly dissipated. The learned helplessness hypothesis explains this particular finding by employing the notion of proactive interference. Proactive and retroactive interference produce memory losses in animals (Maier, Allaway and Gleitman, 1967; Maier and Gleitman, 1967). The effects of both proactive and retroactive interference increase with time and it is possible that first learning control over outcomes could interfere with the retention of the learning that shocks are uncontrollable. Further, there are data which point to retention losses over short periods of time (e.g., D’Amato, 1973 ; Spear, 1973). The aspect of the dog helplessness data that Jay chooses to explain by NE depletion is highly selected. There are five facts about helplessness in the dog which are ignored by the NE depletion view which can he accounted for by the learned helplessness view. Fact I: The time course for NE depletion and recovery falls short of the time course of learned helplessness in the dog by at least an order of magnitude. NE depletion, as we
understand
it, recovers rapidly. The published data suggest that within an hour or two
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MARTIN E. P. SELIGMAN and JAY M. WEBS
after stress, NE has returned to normal (cf. Maynert and Levi, 1964). Interference in the dog, with one session of prior inescapable shock, is certainly present 24 h later, and probabiy 48 h later (Overmier, 1968). That means the phenomenon dissipates sometime between 24 and 72 h after stress. A phenomenon which lasts only up to 2 h does not readily explain a phenomenon which lasts up to 48 h. Fact 2: Multiple sessions of inescapable shock in the dog produce nontransient interference. Seligman and Groves (1970) have shown that the time course of the interference effect is eliminated in dogs if they receive four sessions rather than one session of inescapable shock. The interference effect was evidenced 7 days after their last exposure to inescapable shock. Fact 3: If dogs are raised in the laboratory and deprived of extensive experiences with control over events, only two sessions are required to produce nontransient interference e@cts (Seligman and Groves, 1970). Facts 2 and 3 are consistent with the memory
interpretation of the time course. Repeated exposure to the inescapable stressor (cf. Weiss et al., 1976) seems to cause norepinephrine to recover, and so NE depletion cannot account for these findings. Even if norepinephrine does not recover with repeated exposure to the stressor, a mere lapse of 7 days after inescapable shock should be more than sufficient for norepinephrine recovery in time (cf. Maynert and Levi, 1964). Fact 4: ~nescap~le shock in the dog a$ects dominance one year later. The generality of the interference effect in the dog cannot be explained by the NE depletion hypothesis. Seligman (cited in Seligman, 1975) exposed weanling puppies to escapable, inescapable, or no shock, and tested each triad at one year of age for dominance hierarchies. Every member of each triad was pitted pairwise in a food-competition task. The dogs which received prior exposure to inescapable shock lost in the competition task more often relative to dogs in the controi conditions. This year-long effect which is predicted and explained by the learned helplessness hypothesis is not accounted for by transient norepinephrine deficits. Fact 5: Dogs that learn to escape by standing still are not helpless. Maier’s (1970) classic paper cannot be explained, or can only be explained by straining the NE depletion hypothesis. Maier (1970) exposed dogs to escapable, inescapable, or no shock. For the escape group, the animal was required to remain passive for 2.5 s during shock in order to escape shock. Following this pre-treatment, all dogs were tested in a shuttlebox shock-escape task. If inescapable shock produced motoric inactivation via the mechanism of norepinephrine depletion, then any pre-treatment operation which teaches the animal inactivity ought to severely interfere with its acquisition of an active, instrumental
Fig. I. Mean latency to respond in a shuttle box for dogs previously given training to escape shock by holding still (DRO), given yoked inescapable shocks, or given no shocks. (The yoked group did not learn, whereas the group taught to hold still did learn.) (From S. F. Maier (1970), Failure to escape traumatic shock: Incompatible skeletal motor responses or learned helplessness?, Learning and M#t~v~tio~ 1, 157-170. Copyright 1970 by Academic Press. Reprinted by permission.)
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shock-escape task. The learned helplessness hypothesis makes a contrary assertion. Control over shock, active or passive, is the important psychological dimension which causes interference. Hence, escapably pre-trained animals should acquire the appropriate escape response. Maier’s (I 970) findings confirmed the learned helplessness prediction. Figure 1 shows that animals that first learned to escape passively acquired the shuttle response and were no different from naive controls at the end of testing, whereas inescapably pre-treated dogs showed profound debilitation with learning. It should also be noted that the escape task was acquired over seven daily sessions -a procedure which Jay contends (Weiss et al., 1976) ought to produce no norepinephrine depletion in animals exposed to inescapable shock. In summary, we submit that there are interference effects produced by prior inescap able shock in dogs which are predicted and explained by the learned helplessness hypothesis but are not explained by the NE depletion hypothesis. The rest of the dog data seems explained equally well by either hypothesis, so we prefer the learned helplessness explanation of interference in the dog. We now turn to the evidence on the interference effect in the rat. Evidence from the rat literature
Weiss (Glazer and Weiss, 1976a, b) contends that the interference effect evidenced in the rat following inescapable shock is explained by the learned inactivity hypothesis. Jay has done a very thorough and elegant job of demonstrating that for some of the learned helplessness phenomenon, learned inactivity and NE depletion can explain the data equally as well as the learned helplessness hypothesis. However, we submit that there are 10 sets of findings which cannot be explained by the learned inactivity hypothesis. Fact 1: Degraded contingencies debilitate escape in helpless rats. Learned helplessness in the rat is now a well-documented phenomenon (e.g., Maier, Albin and Testa, 1973 ; Maier and Testa, 1975; Seligman and Beagley, 1975 ; Seligman, Rosellini and Kozak, 1975). The interference effect following exposure to uncontrollable shock in the rat literature affects responses that are gradually acquired by the rat. For example, Seligman and Beagley (1975) reported that if rats are first exposed to inescapable shock and later tested on a simple FR-1 shock-escape response, no deficits are found. If, however, the response requirement is increased so that the bar must be pressed three times (FR-3) in order to escape shock, then the rat which has received prior inescapable shock shows severe debilitation with learning. In contrast, naive rats acquire the escape contingencies quite readily. [Hannum, Rosellini and Seligman (1976) have extended these findings to the developmental history of the rat. Three groups of rats received four sessions of escapable shock, inescapable shock, or no shock shortly after they were weaned. They were tested on an FR-3 lever-press shock-escape task at 90 days of age. Rats which received prior inescapable shock at weaning showed learning deficits. Rats which received prior escapable shock or no shock learned the escape response.] Similarly, Maier and his associates (Maier, Albin and Testa, 1973 ; Maier and Testa, 1975) examined the effects of prior inescapable shock on tasks of differing response requirements and shock-escape contingencies. Maier et al. (1973) reported that rats exposed to inescapable shock usually learn an FR-1 shuttle-box escape response. However, when the response requirement is increased to FR-2, then rats with prior inescapable shock show a marked retardation in learning when compared to rats which received no prior shock or escapable shock. Maier et al. (1973) pointed out that the FR-1 escape appears to be highly reflexive in the rat. However, the FR-2 escape task not only increases the amount of (deliberate) effort required to execute the appropriate response, but also degrades the contingency between the execution of the response and shock termination. Learned inactivity can account for the debilitation in learning the FR-2 shuttle shock-escape and FR-3 lever-press tasks by focusing on the motor activity effort required to execute the task as the locus of the interference effect. The learned helplessness hy-
MARTINE. P. SELIGMANand
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JAY M. WEISS
Fig. 2. Mean FR-3 lever press latencies for rats previously given either inescapable (I) or no (C) shocks and then given noise feedback (F) or no feedback (NF) during lever press escape training (Jackson, Tomie and Maier, 1975). (Tone feedback eliminated failure to escape.) Printed by permission.
pothesis focuses on the degraded contingency as the locus of the interference effect.
between response and shock termination
Fact 2: Increasing feedback from effortful responding breaks up helplessness. Maier and Testa (1975) reported that although inescapably shocked rats failed to learn an ordinary FR-2 shock-escape task, they learn as well as non-shocked controls when there is a 1 s interruption of shock after the first crossing of the FR-2 or when the initial crossing is cued externally. Jackson, Tomie and Maier (1975) reported that feedback in the FR-3 lever-press shock-escape task improves the performance of rats which have received prior inescapable shock. Jackson et al. began by replicating the effect reported by Seligman and Beagley (1975). As shown in Fig. 2, rats which received prior inescapable shock performed poorly on the FR-3 shock-escape response. Another group of inescapable shocked rats. was also tested on the FR-3 lever-press task. However, a 100 ms burst of white noise was presented following each lever-press, thus providing feedback. As can be seen in Fig. 2, these rats learned quite readily. Maier and Testa (1975) degraded the contingency between a single crossing of the shuttle-box and termination of shock by delaying shock termination for 1 or 3 s. Thus, the amount of motor activity required was identical to that of an ordinary FR-I task (which does not show a reliable interference effect), but the contingency was degraded 26-
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Fig. 3. Mean response latency in seconds from onset of onset of conditioned stimulus for the PS and NPS-0. -1. -3, PS-control, and PS-one side groups. PS = pre-shocked, NPS = non-preshocked. (Animals exposed to inescapable shock showed debilitation with learning when a delay in shock termination was superimposed on the FR-I response.) (From S. F. Maier and T. J. Testa (1975), .Failure to learn to escape by rats previously exposed to inescapable shock is partly produced by associative interference, J. camp.physiol. Psycho/. 88. 554-564. Copyright 1975 by the American Psychological Association. Reprinted by permission.)
Learned helplessness, physiological change and learned Inactivity
467
shuttling and shock termination. This delay in shock termination severely retarded the acquisition of the FR-1 shuttle-box escape response in rats previously exposed to inescapable shock, but had no effect on rats not previously exposed to shock (Fig. 3). This finding suggests that the cognitive demands and not the activity demands of the task can produce interference. The learned helplessness hypothesis which asserts that an associative deficit is, in part, responsible for the interference effects predicts and explains these data while learned inactivity does neither. In the Maier et al. (1975) study, shock was presented simultaneously to both chambers of the shuttle-box, so that during the execution of the FR-2 task, there was no consequence of the first component of the FR-2. However, the contingency between shuttle response and shock termination can be made clearer by briefly terminating shock following the first component of the FR-2 or by providing an external cue after the first component. Note that the activity demands remain identical and, if shock termination is very brief following the first component, the duration of shock also remains the same. Fact 3: Immunization does not increase acriuity. Both learned helplessness and learned inactivity hypotheses can explain most of the data on immunization. The learned helplessness hypothesis asserts that prior escape training teaches the animal that it can control shock and hence, when later exposed to inescapable shock, learning that shock is inescapable is proactively interfered with or brought under discriminative control. The learned inactivity hypothesis asserts that during prior escape training the animals learn to be active and this counteracts the inactivity which might be produced by later exposure to inescapable shock. Seligman, Rosellini and Kozak (1975); Maier and Rhoades (cited in Maier and Seligman, 1976); and Williams and Maier (1977) have reported that prior escape training immunizes against the interference effects produced by exposure to inescapable shock. More important, however, is the finding of Williams and Maier (1977) that prior escape training does not cause the animal to be more active during subsequent testing. Rats which received prior escape training did not perform an FR-2 shuttle shock-escape response any better than controls. The immunization account offered by the learned inactivity hypothesis predicts a facilitation in learning in escapably pretreated animals. The learned helplessness account does not, since it is a general responseoutcome learning set which is alleged to mediate immunization. Fact 4: Inescapable shock interferes with learning suppression by punishment. Baker (1976) has reported that rats pre-treated with inescapable shock show interference with learning in a signalled punishment situation. The learned inactivity hypothesis must predict that rats which received prior inescapable shock ought to manifest the learned inactivity sooner than naive controls when later exposed to a shock situation. Hence, facilitation of performance is predicted in a punishment situation following exposure to inescapable shock. Baker (1976), however, reported that rats which received prior inescapable shock did learn more slowly to stop bar-pressing for food in the signalled punishment situation. Jackson, Maier and Rapaport (1978) replicated Baker’s findings and also showed that prior exposure to inescapable shock did not interfere with CER suppression (Fig. 4). These findings are significant for they clearly play off the learned inactivity and learned helplessness accounts against each other. A learned inactivity account predicts equal interference in the acquisition of suppression whether the aversive event is presented contingent upon a response (e.g. a signalled punishment situation) or in the absence of any response-shock contingency (CER). On the other hand, learned helplessness predicts interference only in the signalled punishment situation, since animals should be slower to learn only the relationship between responding and shock. Fact 5: Inducing activirJ* does not reverse interference. Seligman, Maier and Geer (1968) with dogs, Seligman, Rosellini and Kozak (1975) and Seligman and Beagley (1975) with rats, found that escape deficits could be eliminated by forcible exposure to the escape contingency (‘dragging therapy’). Learned inactivity contends that this procedure eliminates the behavioral deficit because the animals are being taught to be active when between
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E. P. SELIGMAN and JAY M. WEISS
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Fig 4. Mean suppression ratio for pre-shocked and restrained rats across blocks of two trials during discriminative punishment conditioning (left panel) and CER conditioning (right panel). (Exposure to inescapable shock affected discriminative punishment conditioning but not CER conditioning.) (From R. L. Jackson, S. F. Maier and P. M. Rapaport (1978). Exposure to inescapable shock produces both activity and associative defects, Learning and Motivation 9, 69-98. Copyright 1978 by Academic Press. Adapted by permission.)
confronted with the aversive stimulus. However, if we examine the performance of a helpless control group which is also being systematically activated by dragging to random locations during exposure to shock but not explicitly exposed to the shock-escape contingency, we fmd continued debilitation with learning. Activation alone is not therapeutic; forced exposure to the escape contingency (or to some other response-outcome contingency; Rosellini and Bazerman, unpublished) is therapeutic. Facts 6, 7, 8 and 9 all deal with transfer of interference beyond shock situations. Learned inactivity is specific to shock: it is learned by pairing with shock termination, and is later elicited by shock. Learned helplessness, however, can be general. The rat is alleged to learn that responding and (some to-be-empirically-defined set of) outcomes are independent (Maier and Seligman, 1976, pp. 39-40), and so interference can be expected across motivators. Fact 6: Interference transfers across aversiveevents.The learned helplessness phenomenon has been demonstrated when the aversive stimulation in both training and testing has been electric shock. In addition, a number of investigators have reported transfer of the interference effect across different aversive outcomes. [Braud, Wepmann and Russo (1969) reported that mice subjected to escapable shock later acquired a water-escape response just as efficiently as naive controls. But inescapably pre-treated mice showed deficits in learning. Altenor, Kay and Richter (1977) reported as much interference with the acquisition of a response to escape from shock or from an underwater maze following either exposure to inescapable shock or underwater submersion.] Rosellini and Seligman (1975) reported transfer from shock to frustration. Three groups of rats received escapable shock, inescapable shock, or no shock after runway training for food reward on a CRF schedule. Once performance had stabilized, extinction was initiated. So, during the extinction procedure, the animals in the three groups ran down an alley for expected food reward but found none. This procedure induces the aversive state of frustration (Wagner, 1969). All groups were then given an opportunity to escape from the frustration-inducing goal box. Rats which received prior escapable shock or no shock escaped from the goal box quite readily. Rats which receieved prior inescapable shock failed to learn to escape from the frustration-inducing situation. In fact, rats which received prior exposure to inescapable shock did not differ from a control group which received no food reward for traversing the alley (Fig. 5). [Prior inescapable shock also reduces shock-elicited aggression in rats. It is a commonly reported phenomenon that if two male rats are present when one is shocked, the rats will engage in fighting. Maier, Anderson and Lieberman (1972) exposed three groups of rats to escapable shock, inescapable, or no shock, and then placed these rats in a shock-elicited aggression situation. Figure 6 shows that shock-elicited aggression was lower in rats which received prior inescapable shock than it was in rats which received prior exposure to escapable shock or no shock.]
Learned helplessness, physiological change and learned inactivity
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Fig. 5. Mean speed to escape a non-rewarded goalbox. (The group designated by E previously received escapable shocks, the group designated by I received inescapable shocks, and the groups designated by C received no shocks. The groups designated by 15 received rewarded runway acquisition training, whereas the group designated by 0 did not. The rats given inescapable shocks (15-I) showed no tendency to escape the frustrating goalbox.) (From Robert A. Rosellini and Martin E. P. Seligman (1973, Frustration and learned helplessness, J. exp. Psychol. Animal Behavior Processes 1, 149-157. Copyright 1975 by the American Psychological Association. Reprinted by permission.)
Fact 7: Noncontingent appetitive outcomes interfere with aversively motivated learning. Joffe, Rawson and Mulick (1973) reared two groups of rats in a contingent and a noncontingent environment. In the contingent environment, food, water and ambient lighting were response dependent. The noncontingent animals received the same food, water and lighting changes, but independently of their behavior. At 60 days of age, all animals were tested for emotionality in an open field. The contingently-reared animals than did the explored more and defecated less, indicating lower emotionality, noncontingently-reared animals, suggesting that lack of control produces more emotional disruption. wight and Katzev (1977) also reported that rats reared in noncontingent environments show shock-escap+avoidanc learning deficits when tested as adults.] Rosellini and Baierman (unpublished) and Goodkin (1976) reported that lack of control over food interferes with subsequent shock-escape learning. Fact 8: Aversive noncontingency retards appetitive learning. There is evidence suggesting that prior exposure to inescapable shock interferes with the acquisition of foodmotivated tasks. Rosellini (1978) reported that rats exposed to inescapable shock showed interference with the acquisition of a food-reinforced lever-press response. Rats exposed to escapable or no shock showed no interference [(Fig. 7). Degrading the response-
Fig. 6. Shock-induced fighting frequency, for each of five test sessions, for rats that had received escapable, yoked inescapable, or no shocks. (Inescapable shocks depressed fighting.) (From Steven F. Maier, Christine Anderson, and David A. Lieberman (1972), Influence of control of shock on subsequent shock-elicited aggression, J. camp. physiol. Psychol. 81, 94-100. Copyright 1972 by the American Psychological Association. Reprinted by permission.)
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Fig. 7. Mean interresponse times (IRTs) in minutes for the escape (E), inescapable (I), and control (C) groups on the first ten responses of the appetitive test in Experiment I. (Animals exposed to inescapable shock took longer to initiate lever-pressing for food reward.) (From R. A. Rosellini (1978), Inescapable shock interferes with the acpuisition of an appetitive operant, Anim. Learng Behau. 6. 155-159. Copyright 1978 by the Psychonomic Society, Inc. Reprinted by permission.)
reinforcer contingency (from a CRF response in Experiment 1 to a CRF with a 1 s delay of reinforcement superimposed in Experiment 2) produced more interference with learning in the inescapably pre-shocked animals. Rapaport and Maier (1978) reported that inescapable shock lowered the rat’s position in a dominance hierarchy as indexed by a food-competition task. Escapable shock did not affect the animal’s position in the hierarchy. The performance of the pre-shocked animals in the food-competition task was not due to decreased appetite or reduced running speed in the test situation following exposure to inescapable shock; for when the animals were tested alone, no debilitation was found. Garber, Fencil-Morse, Rosellini and Seligman (1978) reported that weanling rats given inescapable shock did more poorly as adults in learning appetitive discrimination problems than weanlings given escapable shock or no shock.] Fact 9: Appetitive noncontingency interferes with appetitive learning. Se&man, Meyer and Testa (cited in Seligman, 1975) reported that rats exposed to an operant chamber in which food was delivered on a response-independent basis were slow to acquire responding when food was made response-contingent. [This phenomenon has also been reported by Bainbridge (1973); Eisenberger, Frank, Carlson and Mauriello (1976) in rats; and by Engberg, Hansen, Walker and Thomas (1971); and Welker (1976) in pigeons.] Lack of control over ‘neutral’ stimuli have also been shown to interfere with later learning (Mullins and Winefield, 1977). Further, prior exposure to environments in which food is response-dependent (Rosellini and Bazerman, unpublished) [or exposure to soluble discrimination problems (Mullins and Winefield, 1977)] followed by exposure to inescapable shock (Rosellini and Bazerman) [or insoluble discrimination problems (Mullins and Winefield)] acts as an immunization procedure. That is, there is evidence of appetitive immunization against helplessness. A learned inactivity hypothesis cannot account easily for Facts 6-9. The learned helplessness hypothesis proposes a general cognitive deficit to account for the cross-modal findings. Fact IO: Learned irrelevance. Learned irrelevance is a well-documented phenomenon in rats (Mackintosh, 1973; Baker, 1976). The notion of learned irrelevance is significant, for it documents the rat’s ability to learn that events are independent. Learned helplessness asserts that animals learn that response and outcome are independent during exposure to uncontrollable events, and that this interferes with later learning that responding and outcome are dependent. The feedback from responding is a stimulus event, and so parallel interference should occur for stimuli noncontingently related to outcomes. If Stimulus 1 is presented randomly with respect to some outcome, the lack of contingency between Stimulus 1 and the outcome or event is learned. If, sometime later, Stimulus 1 is paired with an outcome, the animal which has learned the lack of contingency or relationship during prior training will have difficulty making associations between other stimuli and outcomes (Seligman, 1968; Mackintosh, 1973; Baker, 1976). If rats are first
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presented tones randomly interspersed with shocks and then tested for CER suppression to these tones paired with shocks or to lights paired with shocks, conditioning is slower. These phenomena are predicted by the learned helplessness hypothesis, but the learned inactivity hypothesis is obviously silent about them. So ten sets of findings on interference in the rat are predicted by learned helplessness but not learned inactivity. When coupled with our claim (see below) that the rest of the rat literature is explained equally well by learned helplessness or learned inactivity, the learned helplessness view seems a superior explanation of interference in the rat. Philosophical issues
Finally there are also some larger considerations which make us favor the learned helplessness hypothesis over the learned inactivity hypothesis. The first is parsimony. Once we consider the data on the interference effect in humans, parsimony favors learned helplessness hypothesis. The learned helplessness hypothesis, as put forward, tries to explain a range of data in the rat, a range of data in the dog, and an accumulating range of data in humans with one hypothesis. In all of these experiments the same set of operations, that is, the presentation of uncontrollable events, lead to the same results: debilitation with response initiation and debilitation of learning responseoutcome contingencies. We, therefore, infer that it is not unreasonable to think that the same process, learned helplessness, might be at work. Weiss’ position fragments the phenomena into at least three processes. He proposes one explanation for the phenomenon in dogs, another for the phenomenon in rats, and we suppose, yet another for the phenomenon in humans. The processes proposed by Weiss are interesting but, by Occam’s razor, we must prefer a hypothesis which accounts for the phenomena with one process-everything else equal. The learned helplessness hypothesis does just that. So, one philosophical reason for preference of the learned helplessness hypothesis is it provides a general explanation of phenomena across a large range of situations and in at least three species. The second largest consideration stems from stimulus-response vs cognitive positions in learning. Our bias is naked: S-R learning, we believe, is the exception. Higher animals and people usually learn higher order cognitions. There is a strong movement among modem learning theorists (e.g., Mackintosh, 1973 ; Rescorla, 1969; Seligman and Johnston, 1973; and Wagner, 1969) which addresses itself to attention, expectations, memory, and the like-cognitive processes which intervene in rat and human learning. To prefer a response learning hypothesis over a cognitive hypothesis on the grounds that animals cannot have expectations, attention, memory and perceptions requires an anachronistic reading of the major developments in animal leaning of the last 20 years. Our final reason for preferring the learned helplessness hypothesis over the learned inactivity hypothesis is that learned helplessness is not only general to the phenomenon observed in rats, dogs and humans, but it may offer us ways of explaining human depression. One justification of animal experimentation is a concern with understanding and alleviating human misery. Everything else equal, if one hypothesis is applicable to a naturally-occurring human phenomenon (as we believe learned helplessness is to depression), and another is not, the applicable hypothesis ought to be preferred. In summary then, we have argued that on empirical grounds the norepinephrine depletion hypothesis does not explain the interference effects observed in dogs following exposure to uncontrollable shock; while the learned helplessness hypothesis does. We have argued that on empirical grounds, the learned inactivity hypothesis does not explain the phenomenon in rats, while learned helplessness does. Finally we have argued that on philosophical grounds the learned helplessness hypothesis is preferable. Thank you. REFERENCES ALTENORA., KAY E. and RICHTERM. (1977) The generality of learned helplessness Moticafim 8. 54-61.
in the rat. Learning and
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ANISMANH., DE CATANZAROD. and REMINGTON G. (1978) Escape performance following exposure to inescap able shock: Deficits in motor response maintenance. J. exp. Psych& A+nal Behnuior Processes 4, 197-218. BAKER A. G. (1976) Learned irrelevance and learned helplessness: Rats learn that simuii. reinforcers, and responses are uncorrelated. J. exp. Psychol. Animal Behauior Processes 2, 130-141. BAINBRIDGE P. L. (1973) Learning in the rat: Effect of early experience with an unsolvable problem. J. camp. physiol. Psycho/. 82, 301-307. BRAUDW., WEPMANNB. and Russo D. (1969) Task and species generally of the “helplessness” phenomenon. Psychonornic Science 16, I%-1 55. D’AMATOM. (1973) Delayed matching and short-term memory in monkeys. In The Psychology of Learning and Motiuarion (G. H. Bower, Ed.) Vol. 7. Academic Press, New York. EISENBERGER R., FRANK M., CARLSONJ. and MAURIELM J. (1976) Learned industriousness and effort motivation. Unpublished manuscript, State University of New York at Albany. ENGBERGL. A., HANSENG.. WELKERR. L. and THOMASD. R. (1973) Acquisition of key-pecking via autoshaping . as a function of prior experience: “Learned laziness?” Science 178,~1002-1004. _ GARBER J.. FENCIL-MORSEM.. ROSELLINIR. A. and SELIGMANM. ‘E. P. (1978) Inescaoable shock during weanling impairs adult discrimination learning. Behau. Res. Ther. 17, 19%206. . GLAZER H. I. and WEISSJ. M. (1976a) Long-term and transitory interference effects. J. exp. Psychol. Animal Behavior Processes 2, I9 I-201. GLAZERH. I. and WEI~~J. M. (1976b) Long-term interference effect: An alternative to “learned helplessness”. J. exp. Psychol.
Animal
Behavior
Processes
2, 202-213.
HANNUMR. D., RIXELLINIR. A. and SELIGMANM. E. P. (1976) Retention and immunization of learned helplessness from weaning to adulthood. Deul Psycho/. 12, 449-454. HERMANZ. (1970) The effects of noradrenaline on rats’ behavior. Psychopharmacologia 16, 369-374. JACKWNR. L.. MAIER S. F. and RAPAPORTP. M. (1978) Exposure to inescapable shock produces both activity and associative deficits in the rat. Learning and Motivation 9, 69-98. JACKSONR. L.. TOMIEA. and MAIER S. F. (1975) Learned helplessness in rats: EfTects of response produced feedback. Paper presented at Rocky Mountain Psychological Association, Salt Lake City. JOFFEJ. M., RAW~ONR. A. and MULICK J. A. (1973) Control of their environment reduces emotionality in rats. Science 180, 1383-1384. KEL~EYJ. E. (1977) Escape acquisition following inescapable shock in the rat. Anim. Learng Behau. 5, 83-92. MACKINTOSHN. J. (1973) Stimulus selection: Learning to ignore stimuli that predict no change in reinforcement. In Constraints on Learning (R. A. HINDLEand J. STEVENSON-HINDE, Eds.) Academic Press, New York. MAIER S. F. (1970) Failure to escape traumatic shock: Incompatible skeletal motor response or learned helplessness? Learning and Motivation 1. 157-170. MAIER S. F.. ALBIN R. W. and TE~TAT. J. (1973) Failure to learn to escape in rats previously exposed to inescapable shock depends on nature of escape response. 1. camp. physiol. Psycho/. 85, 581-592. MAIERS. F.. ALLAWAYT. A. and GLEITMANH. (1967) Proactive inhibition in rats after prior reversal: A critique of the spontaneous recovery hypothesis. Psychonom. Sci. 9, 63-65. MAIER S. F.. ANDERSONC. and LIEBERMAN D. A. (1972) Influence of control of shock on subsequent shockelicited aggression. J. camp. physiol. Psychol. 81, 94-100. MAIERS. F. and GLEITMANH. (1967) Proactive interference in rats. Psychonom. Sci. 7, 25-26. MAIER S. F. and JACKSONR. L. (1977) The nature of the initial coping response and the learned helplessness effect. Anim. Learns Behau. 5. 407-414. MAIERS. F. and SELIGMANM. E. P. (1976) Learned helplessness: Theory and evidence. J. exp. Psycho/. Genera/ 105. 3-46. MAIER S. F., SELIGMANM. E. P. and SOLOMONR. L. (1969) Pavlovian fear conditioning and learned helplessness. In Punishment (B. A. CAMPBELLand R. M. CHURCH,Eds.) Appleton-Century-Crofts, New York. MAIERS. F. and TESTAT. J. (1975) Failure to learn to escape by rats previously exposed to inescapable shock is partly produced by associative interference. J. camp. physiol. Psychol. 88. 554-564. MILLERN. E. and WEIRSJ. M. (1969) Effects of somatic or visceral responses to punishment. In Punishment and Arersiue Behavior (B. A. CAMPBELL and R. M. CHURCH,Eds.) Appleton-Century-Crofts, New York. MAYNERTE. W. and LEVI R. (1964) Stress-induced release of brain norepinephrine and its inhibition by drugs. J. Pharmac.
exp. Ther.
143, 90-95.
MULLINS G. P. and WINEFIELD4. H. (1977) Immunization and helplessness phenomena in the rat in a nonaversive situation. Anim. Learng Behau. 5, 28-284. OVERMIERJ. B. (1968) Interference with avoidance behavior: Failure to avoid traumatic shock. J. exp. Psychof. 78.340-343.
OVERMIERJ. B. and SELIGMANM. E. P. (1967) Effects of inescapable shock upon subsequent escape and avoidance learning. J. camp. physiol. Psychol. 63, 28-33. RE~CORLAR. A. (1969) Conditioned inhibition of fear. In Fundamental Issues in Associative Learning (N. J. MACKINTOSH and W. K. HONIG, Eds.) Dalhousie University Press, Halifax, Nova Scotia, Canada. RO~ELLINIR. A. and BAZERMANM. (1977) Transfer of learned, helplessness from an,appetitive to an aversive context. Unpublished manuscript. University of Pennsylvania. ROSELLINIR. and SELIGMANM. E. P. (1975) Learned helplessness and escape from frustration. J. exp. Psycho/. Animal
Behavior
Processes
1. 149-158.
SELIGMANM. E. P. (1968) Chronic fear produced by unpredictable shock. J. camp. physiol. Psycho/. 66.402-411. SELIGMANM. E. P. (1975) Helplessness: On depression, deuelopment, and death. Freeman, San Francisco. SELICMANM. E. P. and BEAGLEYG. (1975) Learned helplessness in the rat. J. camp. physiol. Psychol. 88. 534-541. SELIGMANM. E. P. and GROVESD. (1970) Non-transient learned helplessness. Psychonomic Sci. 19. 191-192. SELIGMANM. E. P. and JOHNSTONJ. C. (1973) A cognitive theory of avoidance learning. In Contemporary Approaches to Conditioning and Learning (F. J. MCGUIGANand D. B. LUMSDEN,Eds.) Winston, Washington, D.C.
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M. E. P., MAIER S. F. and GEER J. (1968) The alleviation of learned helplessness in the dog. J. abn.
sot. Psychol. 73, 256-262. SELIGMAN M. E. P., MAIERS. F. and !SOLOMON R. L. (1971) Unpredictable and uncontrollable Aversive Conditioning and Learning (F. R. BRUSH,Ed.) Academic Press, New York.
WILLIAMSJ. L. and MAIER S. F. (1977) Transituational immunization rat. J. exp. Psychol. Animal Behavior Processes 3, 240-253.
B.1I.T
IS 5-H
aversive events. In
and therapy of learned helplessness in the
MARTIN E. P. SELIGMAN and JAY M. WEISS
PART
II:
LEARNED
HELPLESSNESS
MARTIN E. P. SELIGMANand AIDAN ALTENOR* The focus of this presentation will be restricted to a fairly rigorous examination of the data bearing on the three competing theories which have emerged to account for the debilitating effects of prior exposure to inescapable shocks in dogs and rats. The three theories are: (a) learned helplessness (Maier, Seligman and Solomon. 1969 ; Seligman, Maier and Solomon, 1971; Seligman, 1975; Maier and Seligman, 1976); (b) a norepinephrine (NE) depletion hypothesis proposed to account for the interference effects evidenced following exposure to inescapable shocks only in the dog (Weiss, Glazer and Pohorecky, 1976); (c) a learned inactivity hypothesis to account for the deficits evidenced following exposure to inescapable shock only in the rat (Glazer and Weiss, 1976a, b). In this presentation, we will argue (1) that the dog data are explained better by learned helplessness than by the NE depletion view, since five sets of findings, ignored and unaccounted for by the NE depletion view, are accounted for by learned helplessness, whereas all dog data explained by NE depletion are also explained by learned helplessness; and (2) that the rat data are better explained by learned helplessness than learned inactivity, since 10 sets of findings, ignored and unaccounted for by learned inactivity, are accounted for by learned helplessness, whereas all rat data explained by learned inactivity are also explained by learned helplessness. In our response to Professor Weiss’ presentation, we shall argue (3) that Weiss has collected data which are explained by NE depletion and not by learned helplessness, but they are data about the effects of stress per se, not uncontrollable stress; and that (4) Professor Weiss’ learned inactivity data are equally well explained by learned helplessness. Definition of ,hypotheses
The learned helplessness hypothesis (Maier, Seligman and Solomon, 1969; Seligman, Maier and Solomon, 1971; Maier and Seligman, 1976) asserts that during exposure to an uncontrollable outcome, the animal learns of the lack of contingency between its responses and the outcome. That is, it learns that it has no control over the outcome. Such learning produces three deficits. One of these deficits is motivational: dogs and rats which have been exposed to inescapable shocks have a reduced tendency to initiate subsequent escape responding in the presence of shock because part of the incentive for making such responses is the expectation that they will bring relief. If the animal has previously learned that its responses have no effect on relief, this contravenes the expectation. Thus the organism’s motivation to respond is undermined by experience with lack of control. Note that the motivational deficit of the learned helplessness hypothesis has built into it an inactivity notion-the foundation of the learned inactivity hypothesis. There are, in addition, two other effects not postulated by the learned inactivity hypothesis. There is a cognitive deficit: exposure to uncontrollable events interferes with the animal’s ability to learn about contingent relationships between its future behavior and outcomes. In general, if we have acquired a cognitive set in which As are irrelevant to Bs, it will be more difficult to learn that As produce Bs when they do. And, there is an emotional deficit: exposure to uncontrollable events produces greater emotional disruption than exposure to controllable events, first anxiety, then depression. The NE depletion hypothesis which Weiss (Weiss, Glazer and Pohorecky, 1976) has proposed to explain the interference effects in our dogs, and nor in our rats, asserts that * Martin Seligman originally delivered these remarks in live debate with Jay Weiss. Aidan Altenor had a major role in the thinking which went into the debate and into the revision of the transcripts into final written form. Preparation of this paper was supported by a National Institute of Mental Health Grant (MH-19604) to Martin E. P. Se&man and a National Institute of Mental Health Postdoctoral Fellowship (MH-07682) to Aidan Altenor. Martin E. P. Seligman was a fellow at the Center for Advanced Studies in the Behavioral Sciences. Stanford. California. during part of the preparation of this paper.
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inescapable shock produces severe deficiency in central noradrenergic activity. A low norepinephrine level will allow for only a limited amount of motor activity. Following inescapable shock, the activity allowed for by the noradrenergic deficits is insufficient for learning and performing the correct response in shuttle avoidance. Since escapable shock does not produce noradrenergic deficiency, sufficient motor activity can occur for adequate performance on escape and avoidance. The major finding which led Weiss and his colleagues to see a need to postulate NE depletion in dogs was that following one session of inescapable shock, shock-escapeavoidance learning was normal 48 h later (Overmier and Seligman, 1967). Miller and Weiss (1969) originally argued that things that are learned do not disappear in 48 h. Further, there is evidence that a noradrenergic process is involved in the mediation of overt behavior (cf. Herman, 1970), that noradrenergic activity is disrupted by exposure to inescapable shock (Maynert and Levi, 1964), and that the noradrenergic disruption recovers following exposure to inescapable shock (Maynert and Levi, 1964). Hence, exposure to inescapable shock produces a depletion of norepinephrine, which causes motoric inactivation. The resultant NE deficit is transient and the transient effect ob~ined in dogs can be so explained. It should be mentioned that the data summoned by Weiss to explain interference in dogs are obtained from rats. There are no published data examining the time course of NE depletion caused by inescapable shock in the dog. A learned inactivity hypothesis has been generated by Glazer and Weiss (1976a, b) [and, more recently, Anisman, de Catanzaro and Remington (19781-Jto account for the interference effects produced by inescapable shock in the rat. According to this hypothesis, exposure to inescapable shock, particularly long duration shock (5 s or more), results in inactivity in the rat. This is because the rat becomes still during a long shock, and this inactivity is adventitiously paired with shock termination. Weiss and Glazer noted that during long duration shock, there is, early in training, an initial burst of activity with shock onset. This activity declines with continued exposure to shock on a given trial. During repeated exposure to the long duration shock, the rat tends to become inactive much sooner after shock onset, suggesting that the rat learns through adventitious reinforcement to become passive or inactive. This hypothesis suggests that shocks of less than 5 s will not produce interference with subsequent learning to escape shock. It also suggests that if two groups of rats are matched for activity or inactivity, there should be no difference in their subsequent escape learning. Tog evidence unexplained by the NE depletion hypothesis The piece of data from the literature in dogs which Jay Weiss takes as supportive of the NE depletion hypothesis is the finding regarding changes in learned helplessness effects over time. Overmier and Seligman {1967) demonstrated that a single exposure to inescapable shock produced extreme interference or helplessness in 2/3 of the dogs after a 24 h delay. However, after 48 h delay there was only minimal interference after shock exposure. When the animals were tested 72 h later, the effects of learned helplessness had wholly dissipated. The learned helplessness hypothesis explains this particular finding by employing the notion of proactive interference. Proactive and retroactive interference produce memory losses in animals (Maier, Allaway and Gleitman, 1967; Maier and Gleitman, 1967). The effects of both proactive and retroactive interference increase with time and it is possible that first learning control over outcomes could interfere with the retention of the learning that shocks are uncontrollable. Further, there are data which point to retention losses over short periods of time (e.g., D’Amato, 1973 ; Spear, 1973). The aspect of the dog helplessness data that Jay chooses to explain by NE depletion is highly selected. There are five facts about helplessness in the dog which are ignored by the NE depletion view which can he accounted for by the learned helplessness view. Fact I: The time course for NE depletion and recovery falls short of the time course of learned helplessness in the dog by at least an order of magnitude. NE depletion, as we
understand
it, recovers rapidly. The published data suggest that within an hour or two
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after stress, NE has returned to normal (cf. Maynert and Levi, 1964). Interference in the dog, with one session of prior inescapable shock, is certainly present 24 h later, and probabiy 48 h later (Overmier, 1968). That means the phenomenon dissipates sometime between 24 and 72 h after stress. A phenomenon which lasts only up to 2 h does not readily explain a phenomenon which lasts up to 48 h. Fact 2: Multiple sessions of inescapable shock in the dog produce nontransient interference. Seligman and Groves (1970) have shown that the time course of the interference effect is eliminated in dogs if they receive four sessions rather than one session of inescapable shock. The interference effect was evidenced 7 days after their last exposure to inescapable shock. Fact 3: If dogs are raised in the laboratory and deprived of extensive experiences with control over events, only two sessions are required to produce nontransient interference e@cts (Seligman and Groves, 1970). Facts 2 and 3 are consistent with the memory
interpretation of the time course. Repeated exposure to the inescapable stressor (cf. Weiss et al., 1976) seems to cause norepinephrine to recover, and so NE depletion cannot account for these findings. Even if norepinephrine does not recover with repeated exposure to the stressor, a mere lapse of 7 days after inescapable shock should be more than sufficient for norepinephrine recovery in time (cf. Maynert and Levi, 1964). Fact 4: ~nescap~le shock in the dog a$ects dominance one year later. The generality of the interference effect in the dog cannot be explained by the NE depletion hypothesis. Seligman (cited in Seligman, 1975) exposed weanling puppies to escapable, inescapable, or no shock, and tested each triad at one year of age for dominance hierarchies. Every member of each triad was pitted pairwise in a food-competition task. The dogs which received prior exposure to inescapable shock lost in the competition task more often relative to dogs in the controi conditions. This year-long effect which is predicted and explained by the learned helplessness hypothesis is not accounted for by transient norepinephrine deficits. Fact 5: Dogs that learn to escape by standing still are not helpless. Maier’s (1970) classic paper cannot be explained, or can only be explained by straining the NE depletion hypothesis. Maier (1970) exposed dogs to escapable, inescapable, or no shock. For the escape group, the animal was required to remain passive for 2.5 s during shock in order to escape shock. Following this pre-treatment, all dogs were tested in a shuttlebox shock-escape task. If inescapable shock produced motoric inactivation via the mechanism of norepinephrine depletion, then any pre-treatment operation which teaches the animal inactivity ought to severely interfere with its acquisition of an active, instrumental
Fig. I. Mean latency to respond in a shuttle box for dogs previously given training to escape shock by holding still (DRO), given yoked inescapable shocks, or given no shocks. (The yoked group did not learn, whereas the group taught to hold still did learn.) (From S. F. Maier (1970), Failure to escape traumatic shock: Incompatible skeletal motor responses or learned helplessness?, Learning and M#t~v~tio~ 1, 157-170. Copyright 1970 by Academic Press. Reprinted by permission.)
Learned helplessness, physiological change and learned inactivity
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shock-escape task. The learned helplessness hypothesis makes a contrary assertion. Control over shock, active or passive, is the important psychological dimension which causes interference. Hence, escapably pre-trained animals should acquire the appropriate escape response. Maier’s (I 970) findings confirmed the learned helplessness prediction. Figure 1 shows that animals that first learned to escape passively acquired the shuttle response and were no different from naive controls at the end of testing, whereas inescapably pre-treated dogs showed profound debilitation with learning. It should also be noted that the escape task was acquired over seven daily sessions -a procedure which Jay contends (Weiss et al., 1976) ought to produce no norepinephrine depletion in animals exposed to inescapable shock. In summary, we submit that there are interference effects produced by prior inescap able shock in dogs which are predicted and explained by the learned helplessness hypothesis but are not explained by the NE depletion hypothesis. The rest of the dog data seems explained equally well by either hypothesis, so we prefer the learned helplessness explanation of interference in the dog. We now turn to the evidence on the interference effect in the rat. Evidence from the rat literature
Weiss (Glazer and Weiss, 1976a, b) contends that the interference effect evidenced in the rat following inescapable shock is explained by the learned inactivity hypothesis. Jay has done a very thorough and elegant job of demonstrating that for some of the learned helplessness phenomenon, learned inactivity and NE depletion can explain the data equally as well as the learned helplessness hypothesis. However, we submit that there are 10 sets of findings which cannot be explained by the learned inactivity hypothesis. Fact 1: Degraded contingencies debilitate escape in helpless rats. Learned helplessness in the rat is now a well-documented phenomenon (e.g., Maier, Albin and Testa, 1973 ; Maier and Testa, 1975; Seligman and Beagley, 1975 ; Seligman, Rosellini and Kozak, 1975). The interference effect following exposure to uncontrollable shock in the rat literature affects responses that are gradually acquired by the rat. For example, Seligman and Beagley (1975) reported that if rats are first exposed to inescapable shock and later tested on a simple FR-1 shock-escape response, no deficits are found. If, however, the response requirement is increased so that the bar must be pressed three times (FR-3) in order to escape shock, then the rat which has received prior inescapable shock shows severe debilitation with learning. In contrast, naive rats acquire the escape contingencies quite readily. [Hannum, Rosellini and Seligman (1976) have extended these findings to the developmental history of the rat. Three groups of rats received four sessions of escapable shock, inescapable shock, or no shock shortly after they were weaned. They were tested on an FR-3 lever-press shock-escape task at 90 days of age. Rats which received prior inescapable shock at weaning showed learning deficits. Rats which received prior escapable shock or no shock learned the escape response.] Similarly, Maier and his associates (Maier, Albin and Testa, 1973 ; Maier and Testa, 1975) examined the effects of prior inescapable shock on tasks of differing response requirements and shock-escape contingencies. Maier et al. (1973) reported that rats exposed to inescapable shock usually learn an FR-1 shuttle-box escape response. However, when the response requirement is increased to FR-2, then rats with prior inescapable shock show a marked retardation in learning when compared to rats which received no prior shock or escapable shock. Maier et al. (1973) pointed out that the FR-1 escape appears to be highly reflexive in the rat. However, the FR-2 escape task not only increases the amount of (deliberate) effort required to execute the appropriate response, but also degrades the contingency between the execution of the response and shock termination. Learned inactivity can account for the debilitation in learning the FR-2 shuttle shock-escape and FR-3 lever-press tasks by focusing on the motor activity effort required to execute the task as the locus of the interference effect. The learned helplessness hy-
MARTINE. P. SELIGMANand
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JAY M. WEISS
Fig. 2. Mean FR-3 lever press latencies for rats previously given either inescapable (I) or no (C) shocks and then given noise feedback (F) or no feedback (NF) during lever press escape training (Jackson, Tomie and Maier, 1975). (Tone feedback eliminated failure to escape.) Printed by permission.
pothesis focuses on the degraded contingency as the locus of the interference effect.
between response and shock termination
Fact 2: Increasing feedback from effortful responding breaks up helplessness. Maier and Testa (1975) reported that although inescapably shocked rats failed to learn an ordinary FR-2 shock-escape task, they learn as well as non-shocked controls when there is a 1 s interruption of shock after the first crossing of the FR-2 or when the initial crossing is cued externally. Jackson, Tomie and Maier (1975) reported that feedback in the FR-3 lever-press shock-escape task improves the performance of rats which have received prior inescapable shock. Jackson et al. began by replicating the effect reported by Seligman and Beagley (1975). As shown in Fig. 2, rats which received prior inescapable shock performed poorly on the FR-3 shock-escape response. Another group of inescapable shocked rats. was also tested on the FR-3 lever-press task. However, a 100 ms burst of white noise was presented following each lever-press, thus providing feedback. As can be seen in Fig. 2, these rats learned quite readily. Maier and Testa (1975) degraded the contingency between a single crossing of the shuttle-box and termination of shock by delaying shock termination for 1 or 3 s. Thus, the amount of motor activity required was identical to that of an ordinary FR-I task (which does not show a reliable interference effect), but the contingency was degraded 26-
20-
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3 t %
15 -
105-
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I
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Fig. 3. Mean response latency in seconds from onset of onset of conditioned stimulus for the PS and NPS-0. -1. -3, PS-control, and PS-one side groups. PS = pre-shocked, NPS = non-preshocked. (Animals exposed to inescapable shock showed debilitation with learning when a delay in shock termination was superimposed on the FR-I response.) (From S. F. Maier and T. J. Testa (1975), .Failure to learn to escape by rats previously exposed to inescapable shock is partly produced by associative interference, J. camp.physiol. Psycho/. 88. 554-564. Copyright 1975 by the American Psychological Association. Reprinted by permission.)
Learned helplessness, physiological change and learned Inactivity
467
shuttling and shock termination. This delay in shock termination severely retarded the acquisition of the FR-1 shuttle-box escape response in rats previously exposed to inescapable shock, but had no effect on rats not previously exposed to shock (Fig. 3). This finding suggests that the cognitive demands and not the activity demands of the task can produce interference. The learned helplessness hypothesis which asserts that an associative deficit is, in part, responsible for the interference effects predicts and explains these data while learned inactivity does neither. In the Maier et al. (1975) study, shock was presented simultaneously to both chambers of the shuttle-box, so that during the execution of the FR-2 task, there was no consequence of the first component of the FR-2. However, the contingency between shuttle response and shock termination can be made clearer by briefly terminating shock following the first component of the FR-2 or by providing an external cue after the first component. Note that the activity demands remain identical and, if shock termination is very brief following the first component, the duration of shock also remains the same. Fact 3: Immunization does not increase acriuity. Both learned helplessness and learned inactivity hypotheses can explain most of the data on immunization. The learned helplessness hypothesis asserts that prior escape training teaches the animal that it can control shock and hence, when later exposed to inescapable shock, learning that shock is inescapable is proactively interfered with or brought under discriminative control. The learned inactivity hypothesis asserts that during prior escape training the animals learn to be active and this counteracts the inactivity which might be produced by later exposure to inescapable shock. Seligman, Rosellini and Kozak (1975); Maier and Rhoades (cited in Maier and Seligman, 1976); and Williams and Maier (1977) have reported that prior escape training immunizes against the interference effects produced by exposure to inescapable shock. More important, however, is the finding of Williams and Maier (1977) that prior escape training does not cause the animal to be more active during subsequent testing. Rats which received prior escape training did not perform an FR-2 shuttle shock-escape response any better than controls. The immunization account offered by the learned inactivity hypothesis predicts a facilitation in learning in escapably pretreated animals. The learned helplessness account does not, since it is a general responseoutcome learning set which is alleged to mediate immunization. Fact 4: Inescapable shock interferes with learning suppression by punishment. Baker (1976) has reported that rats pre-treated with inescapable shock show interference with learning in a signalled punishment situation. The learned inactivity hypothesis must predict that rats which received prior inescapable shock ought to manifest the learned inactivity sooner than naive controls when later exposed to a shock situation. Hence, facilitation of performance is predicted in a punishment situation following exposure to inescapable shock. Baker (1976), however, reported that rats which received prior inescapable shock did learn more slowly to stop bar-pressing for food in the signalled punishment situation. Jackson, Maier and Rapaport (1978) replicated Baker’s findings and also showed that prior exposure to inescapable shock did not interfere with CER suppression (Fig. 4). These findings are significant for they clearly play off the learned inactivity and learned helplessness accounts against each other. A learned inactivity account predicts equal interference in the acquisition of suppression whether the aversive event is presented contingent upon a response (e.g. a signalled punishment situation) or in the absence of any response-shock contingency (CER). On the other hand, learned helplessness predicts interference only in the signalled punishment situation, since animals should be slower to learn only the relationship between responding and shock. Fact 5: Inducing activirJ* does not reverse interference. Seligman, Maier and Geer (1968) with dogs, Seligman, Rosellini and Kozak (1975) and Seligman and Beagley (1975) with rats, found that escape deficits could be eliminated by forcible exposure to the escape contingency (‘dragging therapy’). Learned inactivity contends that this procedure eliminates the behavioral deficit because the animals are being taught to be active when between
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Fig 4. Mean suppression ratio for pre-shocked and restrained rats across blocks of two trials during discriminative punishment conditioning (left panel) and CER conditioning (right panel). (Exposure to inescapable shock affected discriminative punishment conditioning but not CER conditioning.) (From R. L. Jackson, S. F. Maier and P. M. Rapaport (1978). Exposure to inescapable shock produces both activity and associative defects, Learning and Motivation 9, 69-98. Copyright 1978 by Academic Press. Adapted by permission.)
confronted with the aversive stimulus. However, if we examine the performance of a helpless control group which is also being systematically activated by dragging to random locations during exposure to shock but not explicitly exposed to the shock-escape contingency, we fmd continued debilitation with learning. Activation alone is not therapeutic; forced exposure to the escape contingency (or to some other response-outcome contingency; Rosellini and Bazerman, unpublished) is therapeutic. Facts 6, 7, 8 and 9 all deal with transfer of interference beyond shock situations. Learned inactivity is specific to shock: it is learned by pairing with shock termination, and is later elicited by shock. Learned helplessness, however, can be general. The rat is alleged to learn that responding and (some to-be-empirically-defined set of) outcomes are independent (Maier and Seligman, 1976, pp. 39-40), and so interference can be expected across motivators. Fact 6: Interference transfers across aversiveevents.The learned helplessness phenomenon has been demonstrated when the aversive stimulation in both training and testing has been electric shock. In addition, a number of investigators have reported transfer of the interference effect across different aversive outcomes. [Braud, Wepmann and Russo (1969) reported that mice subjected to escapable shock later acquired a water-escape response just as efficiently as naive controls. But inescapably pre-treated mice showed deficits in learning. Altenor, Kay and Richter (1977) reported as much interference with the acquisition of a response to escape from shock or from an underwater maze following either exposure to inescapable shock or underwater submersion.] Rosellini and Seligman (1975) reported transfer from shock to frustration. Three groups of rats received escapable shock, inescapable shock, or no shock after runway training for food reward on a CRF schedule. Once performance had stabilized, extinction was initiated. So, during the extinction procedure, the animals in the three groups ran down an alley for expected food reward but found none. This procedure induces the aversive state of frustration (Wagner, 1969). All groups were then given an opportunity to escape from the frustration-inducing goal box. Rats which received prior escapable shock or no shock escaped from the goal box quite readily. Rats which receieved prior inescapable shock failed to learn to escape from the frustration-inducing situation. In fact, rats which received prior exposure to inescapable shock did not differ from a control group which received no food reward for traversing the alley (Fig. 5). [Prior inescapable shock also reduces shock-elicited aggression in rats. It is a commonly reported phenomenon that if two male rats are present when one is shocked, the rats will engage in fighting. Maier, Anderson and Lieberman (1972) exposed three groups of rats to escapable shock, inescapable, or no shock, and then placed these rats in a shock-elicited aggression situation. Figure 6 shows that shock-elicited aggression was lower in rats which received prior inescapable shock than it was in rats which received prior exposure to escapable shock or no shock.]
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Fig. 5. Mean speed to escape a non-rewarded goalbox. (The group designated by E previously received escapable shocks, the group designated by I received inescapable shocks, and the groups designated by C received no shocks. The groups designated by 15 received rewarded runway acquisition training, whereas the group designated by 0 did not. The rats given inescapable shocks (15-I) showed no tendency to escape the frustrating goalbox.) (From Robert A. Rosellini and Martin E. P. Seligman (1973, Frustration and learned helplessness, J. exp. Psychol. Animal Behavior Processes 1, 149-157. Copyright 1975 by the American Psychological Association. Reprinted by permission.)
Fact 7: Noncontingent appetitive outcomes interfere with aversively motivated learning. Joffe, Rawson and Mulick (1973) reared two groups of rats in a contingent and a noncontingent environment. In the contingent environment, food, water and ambient lighting were response dependent. The noncontingent animals received the same food, water and lighting changes, but independently of their behavior. At 60 days of age, all animals were tested for emotionality in an open field. The contingently-reared animals than did the explored more and defecated less, indicating lower emotionality, noncontingently-reared animals, suggesting that lack of control produces more emotional disruption. wight and Katzev (1977) also reported that rats reared in noncontingent environments show shock-escap+avoidanc learning deficits when tested as adults.] Rosellini and Baierman (unpublished) and Goodkin (1976) reported that lack of control over food interferes with subsequent shock-escape learning. Fact 8: Aversive noncontingency retards appetitive learning. There is evidence suggesting that prior exposure to inescapable shock interferes with the acquisition of foodmotivated tasks. Rosellini (1978) reported that rats exposed to inescapable shock showed interference with the acquisition of a food-reinforced lever-press response. Rats exposed to escapable or no shock showed no interference [(Fig. 7). Degrading the response-
Fig. 6. Shock-induced fighting frequency, for each of five test sessions, for rats that had received escapable, yoked inescapable, or no shocks. (Inescapable shocks depressed fighting.) (From Steven F. Maier, Christine Anderson, and David A. Lieberman (1972), Influence of control of shock on subsequent shock-elicited aggression, J. camp. physiol. Psychol. 81, 94-100. Copyright 1972 by the American Psychological Association. Reprinted by permission.)
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Fig. 7. Mean interresponse times (IRTs) in minutes for the escape (E), inescapable (I), and control (C) groups on the first ten responses of the appetitive test in Experiment I. (Animals exposed to inescapable shock took longer to initiate lever-pressing for food reward.) (From R. A. Rosellini (1978), Inescapable shock interferes with the acpuisition of an appetitive operant, Anim. Learng Behau. 6. 155-159. Copyright 1978 by the Psychonomic Society, Inc. Reprinted by permission.)
reinforcer contingency (from a CRF response in Experiment 1 to a CRF with a 1 s delay of reinforcement superimposed in Experiment 2) produced more interference with learning in the inescapably pre-shocked animals. Rapaport and Maier (1978) reported that inescapable shock lowered the rat’s position in a dominance hierarchy as indexed by a food-competition task. Escapable shock did not affect the animal’s position in the hierarchy. The performance of the pre-shocked animals in the food-competition task was not due to decreased appetite or reduced running speed in the test situation following exposure to inescapable shock; for when the animals were tested alone, no debilitation was found. Garber, Fencil-Morse, Rosellini and Seligman (1978) reported that weanling rats given inescapable shock did more poorly as adults in learning appetitive discrimination problems than weanlings given escapable shock or no shock.] Fact 9: Appetitive noncontingency interferes with appetitive learning. Se&man, Meyer and Testa (cited in Seligman, 1975) reported that rats exposed to an operant chamber in which food was delivered on a response-independent basis were slow to acquire responding when food was made response-contingent. [This phenomenon has also been reported by Bainbridge (1973); Eisenberger, Frank, Carlson and Mauriello (1976) in rats; and by Engberg, Hansen, Walker and Thomas (1971); and Welker (1976) in pigeons.] Lack of control over ‘neutral’ stimuli have also been shown to interfere with later learning (Mullins and Winefield, 1977). Further, prior exposure to environments in which food is response-dependent (Rosellini and Bazerman, unpublished) [or exposure to soluble discrimination problems (Mullins and Winefield, 1977)] followed by exposure to inescapable shock (Rosellini and Bazerman) [or insoluble discrimination problems (Mullins and Winefield)] acts as an immunization procedure. That is, there is evidence of appetitive immunization against helplessness. A learned inactivity hypothesis cannot account easily for Facts 6-9. The learned helplessness hypothesis proposes a general cognitive deficit to account for the cross-modal findings. Fact IO: Learned irrelevance. Learned irrelevance is a well-documented phenomenon in rats (Mackintosh, 1973; Baker, 1976). The notion of learned irrelevance is significant, for it documents the rat’s ability to learn that events are independent. Learned helplessness asserts that animals learn that response and outcome are independent during exposure to uncontrollable events, and that this interferes with later learning that responding and outcome are dependent. The feedback from responding is a stimulus event, and so parallel interference should occur for stimuli noncontingently related to outcomes. If Stimulus 1 is presented randomly with respect to some outcome, the lack of contingency between Stimulus 1 and the outcome or event is learned. If, sometime later, Stimulus 1 is paired with an outcome, the animal which has learned the lack of contingency or relationship during prior training will have difficulty making associations between other stimuli and outcomes (Seligman, 1968; Mackintosh, 1973; Baker, 1976). If rats are first
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presented tones randomly interspersed with shocks and then tested for CER suppression to these tones paired with shocks or to lights paired with shocks, conditioning is slower. These phenomena are predicted by the learned helplessness hypothesis, but the learned inactivity hypothesis is obviously silent about them. So ten sets of findings on interference in the rat are predicted by learned helplessness but not learned inactivity. When coupled with our claim (see below) that the rest of the rat literature is explained equally well by learned helplessness or learned inactivity, the learned helplessness view seems a superior explanation of interference in the rat. Philosophical issues
Finally there are also some larger considerations which make us favor the learned helplessness hypothesis over the learned inactivity hypothesis. The first is parsimony. Once we consider the data on the interference effect in humans, parsimony favors learned helplessness hypothesis. The learned helplessness hypothesis, as put forward, tries to explain a range of data in the rat, a range of data in the dog, and an accumulating range of data in humans with one hypothesis. In all of these experiments the same set of operations, that is, the presentation of uncontrollable events, lead to the same results: debilitation with response initiation and debilitation of learning responseoutcome contingencies. We, therefore, infer that it is not unreasonable to think that the same process, learned helplessness, might be at work. Weiss’ position fragments the phenomena into at least three processes. He proposes one explanation for the phenomenon in dogs, another for the phenomenon in rats, and we suppose, yet another for the phenomenon in humans. The processes proposed by Weiss are interesting but, by Occam’s razor, we must prefer a hypothesis which accounts for the phenomena with one process-everything else equal. The learned helplessness hypothesis does just that. So, one philosophical reason for preference of the learned helplessness hypothesis is it provides a general explanation of phenomena across a large range of situations and in at least three species. The second largest consideration stems from stimulus-response vs cognitive positions in learning. Our bias is naked: S-R learning, we believe, is the exception. Higher animals and people usually learn higher order cognitions. There is a strong movement among modem learning theorists (e.g., Mackintosh, 1973 ; Rescorla, 1969; Seligman and Johnston, 1973; and Wagner, 1969) which addresses itself to attention, expectations, memory, and the like-cognitive processes which intervene in rat and human learning. To prefer a response learning hypothesis over a cognitive hypothesis on the grounds that animals cannot have expectations, attention, memory and perceptions requires an anachronistic reading of the major developments in animal leaning of the last 20 years. Our final reason for preferring the learned helplessness hypothesis over the learned inactivity hypothesis is that learned helplessness is not only general to the phenomenon observed in rats, dogs and humans, but it may offer us ways of explaining human depression. One justification of animal experimentation is a concern with understanding and alleviating human misery. Everything else equal, if one hypothesis is applicable to a naturally-occurring human phenomenon (as we believe learned helplessness is to depression), and another is not, the applicable hypothesis ought to be preferred. In summary then, we have argued that on empirical grounds the norepinephrine depletion hypothesis does not explain the interference effects observed in dogs following exposure to uncontrollable shock; while the learned helplessness hypothesis does. We have argued that on empirical grounds, the learned inactivity hypothesis does not explain the phenomenon in rats, while learned helplessness does. Finally we have argued that on philosophical grounds the learned helplessness hypothesis is preferable. Thank you. REFERENCES ALTENORA., KAY E. and RICHTERM. (1977) The generality of learned helplessness Moticafim 8. 54-61.
in the rat. Learning and
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