Learned helplessness in the rat.

Four experiments attempted to produce behavior in the rat parallel to the behavior characteristic of learned helplessness in the dog. When rats received escapable, inescapable, or no shock and were later tested in jump-up escape, both inescapable and no-shock controls failed to escape. When bar pressing, rather than jumping up, was used as the tested escape response, fixed ratio (FR) 3 was interfered with by inescapable shock, but not lesser ratios. With FR-3, the no-shock control escaped well. Interference with escape was shown to be a function of the inescapability of shock and not shock per se: Rats that were "put through" and learned a prior jump-up escape did not become passive, but their yoked, inescapable partners did. Rats, as well as dogs, fail to escape shock as a function of prior inescapability, exhibiting learned helplessness.     

习得性无助是习得的吗？——对习得性无助理论及其反思的评述

Seligman和Maier（1967）在动物实验的基础上提出了著名的习得性无助理论,但在2016年,Maier和Seligman二人却联合发文对该理论进行了反思：从最新的神经生物学证据来看,习得性无助的经典理论概括存在基本错误,习得性无助并非习得而来！所谓“习得性”无助,实质上是动物对厌恶刺激长期作用的先天适应性反应,而非认知学习的结果。本文简要梳理习得性无助理论的起源与发展,深入分析这一反思的核心内容、依据及意义,对其中否定习得性无助理论概括的观点,从证据的充分性、研究范式的效度、规范概念等角度作了进行进一步的探讨,并结合新的实验范式对未来研究提出建议。     

Attack, avoidance, and escape reactions to aversive shock

Aversive stimuli are known to produce the behaviors of both escape and attack. The interaction between these two basic reactions was studied with rats and monkeys using many shock-escape and shock-avoidance procedures. All procedures produced attack if a target was present, the attacks occurring shortly after shock delivery. The number of attacks during escape or avoidance was a direct function of the number and duration of shocks received. Consequently, any aspect of the procedure that produced many shocks also produced many attacks such as initial acquisition, extinction, or an increase of the response requirement for escape. The escape tendency acquired prepotency over the tendency to attack since successful escape eliminated attack behavior. The attack tendency retarded escape behavior only during acquisition when the preoccupation with attack precluded the opportunity to learn the escape response. This mutual interference of escape and attack was eliminated when the attack and avoidance tendencies were combined by using biting attack as the shock-avoidance response. The result was unusually rapid conditioning of the biting-attack response. These interactions indicate that both the attack and escape tendency should be considered whenever aversive stimulation is delivered.     

Comparison of behaviors elicited by electrical brain stimulation in dorsal brain stem and hypothalamus of rats.

Four brain-stimulation phenomena elicited from both dorsal brain stem and hypothalamic sites were investigated with the following results: (a) intracranial self-stimulation rate-intensity functions for dorsal brain stem and hypothalamic sites yielded very high (over 1,000 responses/15 min.) to moderate (201-500 responses/15 min.) response rates; (b) d-amphetamine produced higher response rates than either l-amphetamine or saline at both dorsal brain stem and hypothalamic sites, indicating that noradrenergic dorsal brain stem fibers (or cell bodies) support intracranial self-stimulation; (c) dorsal brain stem and hypothalamic self-stimulation sites reliably produced escape behavior; (d) simultaneous stimulation of dorsal brain stem and hypothalamic sites at subthreshold intensities interacted to produce suprathreshold response rates.     

Lesion of the ventral periaqueductal gray reduces conditioned fear but does not change freezing induced by stimulation of the dorsal periaqueductal gray

Previously-reported evidence showed that freezing to a context previously associated with footshock is impaired by lesion of the ventral periaqueductal gray (vPAG). It has also been shown that stepwise increase in the intensity of the electrical stimulation of the dorsal periaqueductal gray (dPAG) produces alertness, then freezing, and finally escape. These aversive responses are mimicked by microinjections of GABA receptor antagonists, such as bicuculline, or blockers of the glutamic acid decarboxylase (GAD), such as semicarbazide, into the dPAG. In this work, we examined whether the expression of these defensive responses could be the result of activation of ventral portion of the periaqueductal gray. Sham- or vPAG electrolytic–lesioned rats were implanted with an electrode in the dPAG for the determination of the thresholds of freezing and escape responses. The vPAG electrolytic lesions were behaviorally verified through a context-conditioned fear paradigm. Results indicated that lesion of the vPAG disrupted conditioned freezing response to contextual cues associated with footshocks but did not change the dPAG electrical stimulation for freezing and escape responses. In a second experiment, lesion of the vPAG also did not change the amount of freezing and escape behavior produced by microinjections of semicarbazide into the dPAG. These findings indicate that freezing and escape defensive responses induced by dPAG stimulation do not depend on the integrity of the vPAG. A discussion on different neural circuitries that might underlie different inhibitory and active defensive behavioral patterns that animals display during threatening situations is presented.     

The debilitating effect of exposure to noncontingent escape: A test of the learned helplessness model

Two studies were conducted to test the hypothesis that exposure to non-contingent escape leads to performance deficits similar to those observed when subjects are exposed to noncontingent aversive outcomes from which there is no escape, and that causal attributions mediate these deficits. Previous attempts to produce “appetitive helplessness” (deficits resulting from exposure to noncontingent positive events) have been plagued by subjects' tendency to believe that they are responsible for positive events. In Experiment 1, 40 subjects were exposed to contingent or noncontingent noise escape trials. As predicted by the learned helplessness model, subjects who received inescapable noise performed less well on a subsequent anagram task than subjects exposed to escapable noise. Similarly, subjects who escaped from the noise owing to the benevolence of a powerful other rather than because of their own efforts, showed performance deficits paralleling those of the inescapable noise subjects. In Experiment 2, subjects who escaped an aversive tone through no effort of their own showed subsequent performance deficits, but globality of their self-reported attributions did not predict subsequent anagram performance. The results of these studies provide support for the hypothesis that uncontrollability, independent of the valence of a particular outcome, is responsible for helplessness deficits, but do not support the mediational role of attributions, at least in the laboratory.     

Frustation and learned helplessness.

This article reports the transfer of learned helplessness from one aversive motivator, shock to another, frustration. In experiment 1, animals were trained to approach food in a runway and concomitantly exposed to either escapable, inescapable, or no shock in a different situation. Extinction was conducted in the runway, and subsequently the animals were tested for hurdle-jump escape from the frustrating goal box. Inescapably shocked rats failed to learn to hurdle-jump, whereas escapably or nonshocked animals learned the frustration escape response. Experiment 2 replicated the basic finidngs of Experiment 1 and showed transfer of learned helplessness from shock to frustration when no running response had been first acquired in the runway.     

Conditioned and unconditioned fear organized in the periaqueductal gray are differentially sensitive to injections of muscimol into amygdaloid nuclei

The lateral and basolateral nuclei of the amygdala (LaA and BLA, respectively) serve as a filter for unconditioned and conditioned aversive information that ascends to higher structures from the brainstem, whereas the central nucleus of the amygdala (CeA) is considered to be the main output for the defense reaction. It has been shown that the dorsal periaqueductal gray (dPAG) is activated by threatening stimuli and has important functional links with the amygdala through two-way anatomical connections. In this work, we examined the influence of chemical inactivation of these nuclei of amygdala on the freezing and escape responses induced by electrical stimulation through electrodes implanted in the dPAG of Wistar rats. Each rat also bore a cannula implanted in the LaA, BLA or CeA for injections of muscimol (0.5 microg/0.5 microL) or its vehicle. The duration of freezing behavior that outlasts electrical stimulation of the dPAG was also measured. On the following day, these animals were submitted to a contextual fear-conditioning using foot shocks as unconditioned stimulus. Conditioned freezing to contextual cues previously associated with foot shocks was also inhibited by injections of muscimol into these amygdaloid nuclei. The contextual conditioned freezing behavior is generated in the neural circuits of conditioned fear in the amygdala. The data obtained also show that injections of muscimol into the three amygdaloid nuclei did not change the aversive threshold of freezing, but disrupted the dPAG post-stimulation freezing. Previous findings that the latter freezing results directly from dPAG stimulation and that it is not sensitive to a context shift suggest that it is unconditioned in nature. Thus, the amygdala can affect some, but not all, aspects of unconditioned freezing. Post-stimulation freezing may reflect the process of transferring aversive information from dPAG to higher brain structures.     

Aversive learning overcomes appetitive innate responding in honeybees

Despite their miniature brain, honeybees have emerged as a powerful model for the study of learning and memory. Yet, they also exhibit innate responses to biologically relevant social signals such as pheromones. Here, we asked whether the bees’ developed learning capabilities allow them to overcome hardwired appetitive responses. Can they learn that attractant pheromones, that are not normally associated with a noxious stimulation in nature, predict the punishment of an electric shock? Immobilized honeybees were trained to discriminate two odorants, one that was paired with a shock and another that had no consequences. We measured whether they learned to produce aversive sting extension responses to the punished but not the non-punished odorant. One odorant was a neutral odor without innate value while the other was either an attractive pheromone (geraniol or citral) or an attractive floral odorant (phenylacetaldehyde). In all cases, bees developed a conditioned aversive response to the punished odorant, be it pheromone or not, and efficiently retrieved this information 1 h later. No learning asymmetries between odors were found. Thus, associative aversive learning in bees is strong enough to override preprogrammed responding, thus reflecting an impressive behavioral flexibility.     

PET activation studies comparing two speech tasks widely used in surgical mapping

"Automatic" speech, especially counting, is frequently preserved in aphasia, even when word production is severely impaired. Although brain sites and processes for automatic speech are not well understood, counting is frequently used to elicit fluent speech during preoperative and intraoperative cortical mapping for language. Obtaining both behavioral and functional brain imaging measures, this study compared counting with a word production task (generation of animal names), including non-verbal vocalizations and quiet rest as control states, in normal and aphasic subjects. Behavioral data indicated that normal and aphasic groups did not differ in counting or non-verbal vocalizations, but did differ significantly in word production ("naming" animals). Functional brain imaging results on normal subjects using partial least squares analysis of PET rCBF images revealed three significant latent variables (LVs): one for naming and vocalizing, identifying bilateral anterior areas, with left predominating over right; a second LV for naming, identifying left and right frontal and temporal areas. For the third, only marginally significant LV, which was associated with automatic speech alone (counting), right and subcortical sites predominated. For patients, two LVs emerged, identified with naming and vocalization, and corresponding to a variety of cerebral sites; the analysis failed to find a specific latent variable for counting. A comparison between group data for normal subjects and patients suggested that the naming, counting, and vocalization tasks were performed differently by the two groups. These results suggest that word generation as a verbal task is more likely to elicit activity in classical language areas than counting. Further studies are suggested to better understand differences between neurological substrates for non-propositional and automatic speech.     

Predatory aggression: Midbrain-pontine junction rather than hypothalamus as the critical structure?

Electrical stimulation of sites in the region of the ventromedial periaqueductal gray substance at the level of the midbrain–pontine junction was found to elicit a predatory attack by a cat upon a rat. The intensity of stimulation required to elicit the attack was three to four times less than that required to elicit similar behavior by hypothalamic stimulation. The results suggest that anatomically distinct regions of the periaqueductal gray substance are concerned with the regulation of predatory and affective forms of aggressive behavior. The difficulty in reconciling these results with the preeminent role assigned the hypothalamus in the organization of predatory behavior is also discussed.     

An experimental analysis of aversive imagery versus electrical aversive conditioning in the treatment of chronic alcoholics

A series of three experiments is described comparing an aversive imagery and an electrical escape conditioning procedure in the treatment of chronic alcoholics. Treatment effects were objectively measured by recording subjects' alcohol consumption in a semi-naturalistic laboratory setting. In contrast to conventional group outcome studies, the use of single-subject methodology provided a fine-grained analysis of individual response patterns. The aversive imagery and escape conditioning methods did not differ from each other, and were relatively ineffective in suppressing alcohol intake. In contrast, a punishment procedure in which shock was contingent on drinking did effectively suppress drinking. The data suggest that alcoholics can control their drinking by self-administered shock. The implications for the analysis and treatment of alcoholics are discussed.     

The effects of hypothermia and hunger on the duration of bar pressing for intracranial self-stimulation in rats

Hypothermic rats at rectal temperatures below 30° C showed decreased duration of bar pressing for intracranial self-stimulation in lateral hypothalamic sites. The same effect was found in hungry rats. Both with cooling and hunger, decreased durations were accompanied by decreased thresholds. The threshold changes in hypothermic rats exceeded 12 μA in some cases. The results are relevant to explanations of why animals turn off rewarding brain stimulation. Particular attention is given to the possibility that cooling enhances neural activity in facilitatory connections between positive and aversive systems.     

Binge eating as escape from self-awareness

This article proposes that binge eating is motivated by a desire to escape from self-awareness. Binge eaters suffer from high standards and expectations, especially an acute sensitivity to the difficult (perceived) demands of others. When they fall short of these standards, they develop an aversive pattern of high self-awareness, characterized by unflattering views of self and concern over how they are perceived by others. These aversive self-perceptions are accompanied by emotional distress, which often includes anxiety and depression. To escape from this unpleasant state, binge eaters attempt the cognitive response of narrowing attention to the immediate stimulus environment and avoiding broadly meaningful thought. This narrowing of attention disengages normal inhibitions against eating and fosters an uncritical acceptance of irrational beliefs and thoughts. The escape model is capable of integrating much of the available evidence about binge eating.     

Reinforcement contrast effects on the rewarding and aversive components of intracranial stimulation

Rats performing a free-operant locomotor response in a shuttlebox to initiate and then escape medial diencephalic stimulation were tested daily on a randomized sequence of three stimulation intensities. In spite of a 1-hr interval between stimulation intensity changes, substantial and graded reinforcement contrast effects were obtained. “Elation” effects were obtained both on the rewarding (latency to initiate) and the aversive (latency to escape) components of stimulation whereas “depression” effects were found only on the measure of reward.     

The reinforcing value of several types of aggressive behavior: A review

Field observations of “surplus killing” and laboratory studies of operant performance rewarded by prey-killing opportunities suggest that predatory behavior is positively reinforcing. Similarly, both repeated encounter and operant performance studies suggest that intraspecific aggression can be positively reinforcing for successful aggressors. While a few studies suggest that defensive aggression under aversive conditions may also be positively reinforcing, it appears that when appropriate response modes are available escape and/or avoidance are preferred to attack. Studies of the reinforcing properties of aggression-eliciting brain stimulation are in general agreement with these conclusions, but methodological problems with these latter observations render them less compelling. The progressive escalation of aggression seen in “warm-up effects” of birds and fish, “priming effects” of mice, and ecstatic violence of humans may be analogous processes based on the positively self-reinforcing characteristics of some kinds of aggression. The transient reductions of aggression which appear as refractory periods and satiation effects in a variety of species may reflect temporary reductions in the reinforcing value of aggression. All these temporal effects must be considered in the evaluation of experiments on the reinforcing value of aggression. More generally, it is possible that these temporal fluctuations reflect the operation of common motivational processes (aggressive states) which regulate overt aggression by changing its reinforcing value.     

Persistence training: a partial reinforcement procedure for reversing learned helplessness and depression

This article examines the relative merits of either partial or continuous (total) success therapy as a device for reversing learned helplessness and depression in humans. College students experienced (a) no treatment followed by either abbreviated (20 trials) or extended (40 trials) continuous success therapy, (b) soluble problems followed by either abbreviated or extended continuous success therapy, (c) insoluble problems followed by either abbreviated or extended continuous success therapy, or (d) insoluble problems followed be either abbreviated or extended partial success therapy. Subsequently, subjects in all eight groups received 40 escape-extinction trials in which aversive tones were not controllable. The results of this experiment indicated that both continuous and partial success schedules were effective in reversing depressed responding (helplessness) induced by prior exposure to insoluble problems. However, only the partial success therapy schedules produced persistent escape responding in extinction. Also, across therapy procedures, extended therapy generated more response persistence in escape extinction than did abbreviated therapy. Theoretical implications of these results are discussed, and a compatible new treatment program, labeled persistence training, is introduced.     

Basolateral amygdala inactivation impairs learned (but not innate) fear response in rats

Numerous studies have suggested that the amygdala is involved in the formation of aversive memories, but the possibility that this structure is merely related to any kind of fear sensation or response could not be ruled out in previous studies. The present study investigated the effects of bilateral inactivation of the amygdaloid complex in rats tested in the plus-maze discriminative avoidance task. This task concomitantly evaluates aversive memory (by discrimination of the two enclosed arms) and innate fear (by open-arm exploration). Wistar rats (3-5 months-old) were implanted with bilateral guide cannulae into basolateral amygdala. After surgery, all subjects were given 1 week to recover before behavioral experiments. Afterwards, in experiment 1, 15 min prior to training, 0.5 μl of saline or muscimol (1 mg/ml) was infused in each side via microinjection needles. In experiment 2 the animals received injections immediately after the training session and in experiment 3 rats were injected prior to testing session (24 h after training). The main results showed that (1) pre-training muscimol prevented memory retention (evaluated by aversive arm exploration in the test session), but did not alter innate fear (evaluated by percent time in open arms); (2) post-training muscimol impaired consolidation, inducing increased percent in aversive arm exploration in the test session and (3) pre-testing muscimol did not affect retrieval (evaluated by aversive enclosed arm exploration in the test session). The results suggest that amygdala inactivation specifically modulated the learning of the aversive task, excluding a possible secondary effect of amygdala inactivation on general fear responses. Additionally, our data corroborate the hypothesis that basolateral amygdala is not the specific site of storage of aversive memories, since retention of the previously learned task was not affected by pre-testing inactivation.     

The influence of stimulus intensity and motivational differences on learned helplessness deficits

Two experiments are reported which assess the moderating effects on learned helplessness deficits of individual differences in task-specific motivation and expectation of control. In Experiment 1 a neutral stimulus was used and in this case only high motivation subjects displayed helplessness deficits in response to noncontingency training. In addition, high motivation subjects demonstrated greater sensitivity to the noncontingency than did low motivation subjects. However, when an aversive stimulus was used in Experiment 2 the moderating effect of motivational differences was removed and this was accompanied by greater sensitivity to the noncontingency on the part of low motivation subjects. Indeed, the learned helplessness effect in Experiment 2 was more pronounced within the low motivation group. The theoretical significance of these findings is explored and directions for future research are suggested.     

Learned preferences induced by electrical stimulation of a food-related area of the parabrachial complex: effects of naloxone

Electrical stimulation of the External Lateral Parabrachial Subnucleus (LPBe), a food-related area, induced behavioral preferences for associated stimuli in a taste discrimination learning task. Although this stimulation appeared to be ineffective to elicit standard lever press self-stimulation, it induced place preference for one of two training compartments of a rectangular maze in which animals (adult male Wistar rats) received concurrent electrical brain stimulation. In subjects that consistently showed a preference behavior in different trials, administration of the opioid antagonist naloxone (4 mg/ml/kg) blocked concurrent learning when the test was made in a new maze but not in the same maze in which animals had learned the task. These results are discussed in terms of the possible participation of the LPBe subnucleus in different natural and artificial brain reward systems.