Learned helplessness in the rat: Time course, immunization, and reversibility.

Previous research has shown that rats, like dogs, fail to escape following exposure to inescapable shock. 3 experiments were conducted with a total of 121 male Sprague-Dawley rats to further explore parallels between rat and dog helplessness. The failure to escape did not dissipate in time; Ss failed to escape 5 min, 1 hr, 4 hrs, 24 hrs, and 1 wk after receiving inescapable shock. Ss that first learned to jump up to escape were not retarded later at barpressing to escape following inescapable shock. Failure to escape could be broken up by forcibly exposing the S to an escape contingency. Therefore, the effects of inescapable shock in the rat parallel learned helplessness effects in the dog. (23 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cross-stressor immunization against the behavioral deficits introduced by uncontrollable shock.

In 4 experiments with 204 male CD-1 mice, exposure to inescapable shock disrupted performance in both shock- (SE) and water-escape (WE) tasks. These deficits were prevented in Ss that were previously trained in the same task. However, an asymmetrical immunization effect was seen in a cross-stressor paradigm. Whereas deficits of WE performance engendered by inescapable shock were prevented by prior SE training, the deficits of SE were not eliminated by prior WE training. Evidently, the immunization effect occurs when initial training and subsequent testing are conducted in the same task or when the initial training and uncontrollable stress session involve the same aversive stimulus. Norepinephrine (NE) determinations revealed that reductions of NE introduced by inescapable shock were unaffected by prior SE training and were enhanced by prior exposure to the stress of water immersion. Thus, although the performance deficit introduced by inescapable shock may be related to variations of NE, the immunization effect probably was unrelated to alterations of NE. Data provisionally suggest that the immunization stems from 2 independent factors: Initially training Ss in an active escape task may (a) disrupt subsequent learning that the inescapable stress actually is uncontrollable and (b) limit the influence of the motor deficits introduced by uncontrollable shock on subsequent escape performance. (28 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Ventromedial septal lesions in rats reduce the effects of inescapable shock on escape performance and analgesia.

In 2 experiments with 104 male Sprague-Dawley rats, lesions of the ventromedial septum (VMS) reduced or eliminated several effects of exposure to inescapable shock, but lesions of the dorsolateral septum did not. Exp I demonstrated that VMS lesions reduced the loss in body weight produced by inescapable shock and eliminated the subsequent (24 hrs later) interference with escape performance (learned helplessness). Exp II demonstrated that VMS lesions reduced the analgesia that occurs immediately following inescapable shock and the analgesia reinstated by exposure to escapable shock 24 hrs later. Findings indicate that VMS lesions reduce several responses to inescapable shock and suggest the possibility that all of these effects may reflect a unitary deficit. It is hypothesized that VMS lesions reduce these effects of exposure to inescapable shock either by reducing the ability of the rats to learn that their responses and shocks were uncorrelated or by reducing the emotional impact of this lack of correlation. (52 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The Kamin effect as a function of number of prior unsignaled inescapable shocks.

3 groups of 30 naive male albino Sprague-Dawley rats received 1, 5, or 10 unsignaled inescapable shocks either .02, 2.5, 4, 10, or 24 hrs prior to 1-way avoidance training. For each phase an additional 6 Ss were assigned to a no-shock control group. Trials to criterion in avoidance learning were a nonmonotonic function of time since prior inescapable shock; poorest performance was shown at intermediate shock-acquisition intervals. The locus of maximum performance decrement shifted to longer intervals with increasing numbers of prior inescapable shocks. Also, variability in performance increased, then decreased, as a function of time since inescapable shock in a manner parallel to the changes in performance means. Findings indicate that unsignaled inescapable shock is sufficient to produce Kaminlike effects. (15 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Escape performance after inescapable shock in selectively bred lines of mice: Reponse maintenance and catecholamine activity.

Examined the effects of inescapable shock on subsequent escape performance and shock-elicited activity in 6 lines of mice (a total of 528 Ss in 6 experiments) selectively bred for differences in general locomotor activity. The line differences in locomotor activity were found to be unrelated to the differences observed on shock-elicited activity. However, escape performance following exposure to inescapable shock was predictable from the levels of shock-elicited activity. Those lines that displayed the greatest decline in motor activity during shock likewise displayed the most pronounced escape deficits. The line differences in escape performance induced by inescapable shock could be mimicked by treatment with a tyrosine hydroxylase inhibitor, alpha-methylparatyrosine. As predicted, the lines that displayed the least interference after tyrosine hydroxylase inhibition exhibited the smallest reduction in levels of catecholamines. The effects on escape performance following inescapable shock are interpreted in terms of the role of response maintenance deficits produced by catecholamine depletion. (18 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Shock controllability and the nature of stress-induced analgesia.

Three experiments, with 160 male albino rats, examined the impact of the escapability of shock on the nature of the analgesia produced by shock. In Exp I, Ss were exposed to 0, 20, 40, or 80 escapable or yoked inescapable shocks. Tailflick testing revealed a double-peak pattern in which analgesia was present after 20 and 80 shocks for both escapable and inescapable shock. Analgesia after 20 escapable or inescapable shocks was insensitive to subcutaneous naltrexone (14 mg/kg), as was the analgesia after 80 escapable shocks. However, the analgesia after 80 inescapable shocks was completely blocked by naltrexone. In Exp II, the analgesia following 80 inescapable shocks persisted for at least 2 hrs, whereas it dissipated rapidly following 80 escapable shocks. The analgesia produced by escapable shock even dissipated with the continued occurrence of escapable shock. Shock controllability altered the analgesia produced by subsequent exposure to shock. Prior experience with controllable shock completely blocked the late-appearing naltrexone reversible analgesia; prior experience with uncontrollable shock led it to appear sooner. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Shock controllability and opioid substrates of escape performance and nociception: Differential effects of peripherally and centrally acting naltrexone.

In 2 experiments with 104 male albino rats, Ss exposed to inescapable shock (IS) exhibited analgesia and a significant impairment of shock-escape learning in a shuttlebox situation 24 hrs later. In contrast, Ss exposed to escapable shock (ES) or to no shock (NS) displayed neither effect. Subcutaneous naltrexone HCl (10 mg/kg) significantly reduced the analgesia and completely eliminated the escape deficit in IS Ss, but it induced hyperalgesia and hampered escape performance in ES and NS Ss. The same dose of naltrexone methylbromide (quaternary naltrexone), which has low ability to cross the blood-brain barrier, had no effect on either the antinociception or the escape deficit produced by IS, although it also induced escape impairment and hyperalgesia in Ss preexposed to ES or to NS. Both the escape interference and the antinociceptive consequences of IS could be reduced partially by a much lower dose (1 mg/kg) of naltrexone, but 50 times this amount of quaternary naltrexone was still without effect. Results imply that the consequences of exposure to IS are mediated by activation of central opioid processes, whereas naltrexone-induced effects in ES and NS Ss may be peripherally mediated. (64 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cue and response-choice acquisition and reversal after exposure to uncontrollable shock: Induction of response perseveration.

Evaluated the effects of inescapable shock in shock-motivated cue, response-choice (RC), and RC/positional Y-maze discrimination tasks. Ss were 253 male CD-1 mice. In the RC paradigm, Ss were required to turn in a predetermined direction to escape, whereas in the RC/positional task, Ss were required to enter the arm to the right of the start arm on any given trial. Although inescapable shock retarded escape performance, this was dependent on task difficulty and on the compatibility between response tendencies and the response requirement of the task. Irrespective of the task, exposure to inescapable shock did not influence accuracy of discrimination responding (acquisition or performance of a previously established discrimination). Likewise, discrimination reversal performance was unaffected by inescapable shock in either the cue or the RC paradigm. In contrast, acquisition of the RC/positional reversal was retarded by inescapable but not escapable shock. (39 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The role of the amygdala and dorsal raphe nucleus in mediating the behavioral consequences of inescapable shock

It has been argued that exposure to inescapable shock produces later behavioral changes such as poor shuttle box escape learning because it leads to the conditioning of intense fear, which later transfers to the shuttle box test situation and interferes with escape. Both fear, as assessed by freezing, and escape were measured in Sprague-Dawley rats 24 hr after exposure to inescapable shock. Lesions of the basolateral region and central nucleus of the amygdala eliminated the fear that transfers to the shuttle box after inescapable shock, as well as the fear conditioned in the shuttle box by the shuttle box shocks. However, the amygdala lesions did not reduce the escape learning deficit produced by inescapable shock. In contrast, dorsal raphe nucleus lesions did not reduce the fear that transfers to the shuttle box after inescapable shock, but eliminated the enhanced fear conditioning in the shuttle box as well as the escape deficit. The implications of these results for the role of fear and anxiety in mediating inescapable shock effects are discussed.     

Dissociation of long-term analgesia and the shuttle box escape deficit caused by inescapable shock.

Previous studies indicate that inescapably shocked rats perform poorly on a 2-way shuttlebox escape task 24 hrs after shock. Because inescapably shocked rats become analgesic upon reexposure to a small amount of shock 24 hrs after inescapable shock (IS), they are likely to be analgesic during the shuttlebox escape task. Ss receiving an equivalent amount of escapable shock display neither the escape deficit nor the analgesia. Both the analgesia and the escape deficit respond in a similar fashion to the manipulation of a variety of other variables. These findings have led to the suggestion that the analgesia (long-term analgesia) may cause the IS-produced escape deficit. However, the present 2 experiments with 72 male albino rats demonstrated that 2 pituitary manipulations that completely eliminate the analgesia have no effect on the escape deficit. Both hypophysectomy and dexamethasone administration blocked the analgesic consequences of IS but did not reduce the magnitude of the escape deficit. Therefore, the long-term analgesia produced by IS does not cause the deficit in shuttlebox escape performance displayed by inescapably shocked rats. Results indicate that the pituitary is not essential in the production of this escape deficit. (47 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Exposure to uncontrollable stress alters withdrawal from morphine.

Examined the influence of the controllability/uncontrollability of shock as a stressor on the severity of subsequent morphine withdrawal in 2 experiments with 84 male Holtzman rats. In Exp I (36 Ss), Ss that received 2 daily sessions of 80 yoked-inescapable shocks, in contrast to those given 80 escapable shocks or restrained without shock, showed an enhanced series of correlated withdrawal behaviors (i.e., mouthing, teeth chattering, head/body shakes) 24 hrs later when injected with morphine sulfate (5 mg/kg) followed by a naloxone HCl (5 mg/kg) challenge. In Exp II (48 Ss), this finding was replicated with escape-yoked-restrained Ss given saline injections during the pretreatment phase, but the impact that inescapable shock had on later precipitated withdrawal was completely blocked when Ss were administered naltrexone HCl (14 mg/kg) before each shock session. Findings are discussed in terms of the capability of inescapable shock to activate an endogenous opiate system, thereby leading to a sensitization of release or receptor processes that could protentiate later morphine withdrawal. (56 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Failure to learn to escape in rats previously exposed to inescapable shock depends on nature of escape response.

Results of previous studies show that dogs exposed to inescapable shocks in a Pavlov harness subsequently fail to learn to escape shock in a shuttle box. The present 6 experiments attempted to replicate this finding with male Sprague-Dawley rats (N = 182). In agreement with many previous investigations, Exp I found that Ss exposed to inescapable shock did not fail to learn to escape in a shuttle box. Exp II, III, and IV varied the number, intensity, and temporal interval between inescapable shocks and did not find failure to learn in the shuttle box. An analysis of responding in the shuttle box revealed that Ss shuttled rapidly from the very 1st trial, whereas dogs acquire shuttling more gradually. Exp V and VI revealed that Ss exposed to inescapable shock failed to learn to escape when the escape response was one that was acquired more gradually. Exp V utilized a double crossing of the shuttle box as the escape response and Exp VI utilized a wheel-turn response. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Failure to learn to escape by rats previously exposed to inescapable shock is partly produced by associative interference.

2 experiments demonstrated that the effects of prior exposure to inescapable shock on the subsequent acquisition of an escape response in rats is determined by the nature of the contingency that exists between responding and shock termination during the escape learning task, and not by the amount of effort required to make the response or the amount of shock that the S is forced to receive during each trial. Exp I, using 48 male Simonsen rats, showed that inescapably shocked Ss did not learn to escape shock in a shuttle box if 2 crossings of the shuttle box were required (fixed ratio, FR, -2) to terminate shock, but did learn this FR-2 response if a brief interruption of shock occurs after the 1st crossing of the FR-2. Exp II with 72 Ss showed that inescapably shocked Ss learned a single-crossing escape response as rapidly as did controls, but were severely retarded if a brief delay in shock termination was arranged to follow the response. Results are discussed in terms of the learned helplessness hypothesis, which assumes that prior exposure to inescapable shock results in associative interference. (15 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Learned helplessness in the gerbil?

27 male Mongolian gerbils were assigned to escapable, inescapable, and control groups and subjected to 2 consecutive days of jump-up escape followed 24 hrs later by testing in a barpress escape task. Reliable differences occurred between escapable and inescapable Ss and between inescapable and control Ss. Findings provide evidence of learned helplessness in Mongolian gerbils. (14 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

DSP4 (N-2-chloroethyl-N-ethyl-2-bromobenzylamine), a new noradrenaline neurotoxin, and stimulus conditions affecting acquisition of two-way active avoidance.

Several CS and UCS variables known to affect the rate of acquisition of the 2-way active avoidance task were investigated in rats treated with the novel selective noradrenaline neurotoxin DSP4 (50 mg/kg, ip). 234 male Sprague-Dawley rats were used in 6 experiments. Although the DSP4 Ss did not demonstrate the linear relation between CS duration and avoidance acquisition to the same extent as controls, their avoidance performance was as drastically disrupted as that of the controls both by preexposure to the CS and by increasing levels of shock intensity. DSP4 Ss also evidenced fear retention for the shuttle box cues previously associated with inescapable shocks to as marked a degree as control Ss. Biochemical data indicated profound noradrenaline depletion in the cortex and hippocampus and a lesser depletion in the hypothalamus. Findings offer a behavioral characterization of the consistent DSP4-induced impairment of 2-way active avoidance acquisition. (46 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Escape/avoidance responding in rats depends on strain and number of inescapable preshocks.

2 experiments examined escape-avoidance responding in a 1-way jump box following exposure to signaled, inescapable shock. In Exp I with 24 female Long-Evans rats, the occurrence of failures to escape and to avoid was an increasing function of the number of preshocks, over a range of 75-275, with a pronounced interference effect occurring after 225 and 275 preshocks. In Exp II with 10 Long-Evans (noninbred) and 10 Fischer (inbred) female rats, there were large differences between strains in failures both to escape and to avoid following 225 preshocks. Long-Evans Ss were severely retarded, whereas Fischer Ss were disrupted only during the initial trials. Findings demonstrate the importance of strain and number of preshocks in controlling the interference effect in rats. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The noradrenergic system of the amygdala and aversive information processing.

In 4 experiments, 113 water-deprived male Long-Evans rats were trained to drink in a passive avoidance apparatus. After reaching a latency criterion, Ss were given a single 3-sec, 3-mA footshock. Immediately or 12 hrs after footshock, Ss were given intracranial injections of vehicular saline, norepinephrine (NE), propranolol, or dopamine (DA) into the amygdala, internal capsule, lateral ventricles, or caudate-putamen. Ss were tested for passive avoidance at 30 min or 24 hrs following footshock. No memory deficits were seen as a consequence of short-term retention or because of proactive or toxicity effects. Retention deficits were seen in the 24-hr test only in Ss injected with NE in the amygdala, internal capsule, or lateral ventricles. However, qualitative differences in stress-indicative behaviors were noted in the NE groups and in the DA-amygdala Ss. Results suggest that the noradrenergic system of the amygdala is involved in the long-term processing of the emotional attributes of aversive information. (66 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of amygdala, hippocampus, and periaqueductal gray lesions on short- and long-term contextual fear.

Examines the effects of amygdala, hippocampus, and periaqueductal gray (PAG) lesions on contextual fear conditioning in 48 female rats. Freezing behavior served as the measure of conditioning. Unlesioned control Ss showed reliable conditional freezing in the testing chamber when observed both immediately and 24 hrs after footshocks. In contrast, Ss with amygdala or ventral PAG lesions exhibited a significant attenuation in freezing both immediately and 24 hrs after the shocks. Dorsal PAG lesions had no effect on freezing at either time. Ss with hippocampal lesions displayed robust freezing behavior immediately following the shock, even though they showed a marked deficit in freezing 24 hrs after the shock. These results indicate that there are anatomically dissociable short- and long-term conditional fear states. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Learned helplessness in the rat.

4 experiments, using a total of 159 male albino Sprague-Dawley rats, attempted to produce behavior in the rat parallel to the behavior characteristic of learned helplessness in the dog. When Ss received escapable, inescapable, or no shock and were later tested in jump-up escape, both inescapable and no-shock controls failed to escape. When barpressing, 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 a function of the inescapability of shock and not shock per se: Ss that were "put through" and learned a prior jump-up escape did not become passive, but their yoked, inescapable partners did. It is concluded that rats, as well as dogs, fail to escape shock as a function of prior inescapability, exhibiting learned helplessness. (24 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Fear conditioned with escapable and inescapable shock: Effects of a feedback stimulus.

Four experiments, with 140 male Fischer rats, compared the level of fear conditioned with escapable and inescapable shock. In Exps I and II, master Ss that had received 50 unsignaled escapable shocks were less afraid of the situation where the shock had occurred than were yoked Ss that had received inescapable shocks. Comparable results were found in Exps III and IV, which used freezing as an index of fear of a discrete CS that had been paired with shock. Control per se was not necessary to produce the low level of fear seen in the master Ss. Yoked groups receiving a feedback signal at the time the master made an escape response showed a low level of fear that was comparable to that of the masters and significantly less than that seen in the yoked Ss without feedback. In addition, there were strong suggestions that control and feedback exert their effects through the same or highly similar mechanisms. Possible explanations for how control and the exteroceptive feedback signal produce this effect are discussed. (35 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)