Philip J. Bersh

Interaction of Pavlovian conditioning with a zero operant contingency: chronic exposure to signaled inescapable shock maintains learned helplessness effects.

In four experiments we used triads, consisting of escapable-shock (ES), yoked inescapable-shock (IS), and no-shock (NS) rats, to investigate the effect of the interaction between Pavlovian contingencies and a zero operant contingency (i.e., uncontrollability) upon subsequent shock-escape acquisition in the shuttle box. After exposure to 50 signals and shocks per session for nine sessions, interference with shuttle box escape acquisition for IS rats was a monotonically increasing function of the percentage of signal-shock pairings during training (Experiment 1), with 50% pairings producing little or no impairment. Without regard to signaling, ES rats performed as well as NS rats. Experiment 2 demonstrated that our training and test conditions led to substantial and equal impairment in IS rats preexposed for one session to 100% or 50% signal-shock pairings or to unsignaled shocks. In Experiment 3, chronic exposure to 100% signaled inescapable shocks resulted in impairment only if the signal (light) was present during the shuttle box test. The continuous presence of the signal during the test contrasted with its discrete (5-s) presentation during training and suggested that an antagonistic physiological reaction rather than a specific competing motor response had been conditioned. Experiment 4 provided evidence for possible conditioned opioid mediation by demonstrating contemporaneous stress-induced analgesia and shock-escape impairment in IS rats chronically exposed to 100%, but not to 50%, signal-shock pairings, and the elimination of both analgesia and escape interference by the opiate antagonist naltrexone. Thus, chronic exposure to uncontrollable shocks appears to maintain the impairment produced by acute exposure only if the shocks are adequately signaled.

Signals for shock-free periods during chronic exposure to delayed-escapable and inescapable shocks: effects on later escape acquisition

Abstract Two experiments investigated the acquisition of shock-escape responses in an illuminated shuttlebox following chronic exposure to shock that was escapable after a 2-s delay (ES) and to yoked inescapable shock (IS) under conditions in which 5-s house-light presentations signaled shock-free periods (CS−) of variable duration. Experiment 1 found that IS rats, as well as a number of ES rats, exposed to this treatment showed impaired shuttlebox escape performance, while a control procedure involving an equal percentage of paired and explicitly unpaired signals and shocks yielded performance that was nearly comparable to that of shock-naive rats. Experiment 2 retained the CS− signal condition while studying the contribution of the escape-delay requirement to the impaired shuttlebox escape performance of ES rats in the preceding experiment. Here it was found that escape deficits again occurred for ES rats trained previously with the 2-s escape delay, but not for ES rats permitted immediate escape from shock during training. The respective yoked IS groups displayed comparable impairment in the shuttlebox. Thus, in opposition to the ameliorative effect of a shock-termination feedback stimulus, explicitly unpaired presentations of signals and shocks maintained the disruptive effects of inescapable shock over multiple sessions and increased the impact on ES rats of brief periods of uncontrollability embedded in escape-delayed shocks.

Opiate antagonists overcome the learned helplessness effect but impair competent escape performance.

Rats exposed to inescapable shocks exhibited deficiencies in learning to escape shock in a novel situation 24 hours later (learned helplessness). Opiate antagonists (naloxone or naltrexone) blocked the learned helplessness effect, allowing efficient escape performance on the subsequent test. In contrast, these drugs impaired the performance of rats pretrained with escapable shocks and animals with no previous exposure to shock. Both effects occurred at small doses and increased substantially with higher doses. The results suggest a significant role for endogenous opiates in the induction of learned helplessness as well as in the acquisition of efficient escape behavior.

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

Rats exposed to inescapable shock exhibited analgesia and a significant impairment of shock-escape learning in a shuttle box situation 24 hr later. In contrast, rats exposed to escapable shock or to no shock displayed neither effect. Naltrexone (10 mg/kg) significantly reduced the analgesia and completely eliminated the escape deficit in inescapably shocked rats but induced hyperalgesia, coupled with a marked deterioration of escape performance, in escapably shocked and nonshocked rats. The same dose of 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 inescapable shock, although it also induced escape impairment and hyperalgesia in rats preexposed to escapable shock or to no shock. A second experiment demonstrated that both the escape interference and the antinociceptive consequences of prior inescapable shock 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. These results imply that the consequences of exposure to inescapable shock are mediated by activation of central opioid processes whereas naltrexone-induced effects in escapably shocked and nonshocked animals may be peripherally mediated. The relevance of these findings to the possible role of nociception in escape performance is discussed.

Eysenck's theory of incubation: a critical analysis.

Abstract Eysencks theory of incubation is summarized. Arguments and evidence concerning its validity and potential value are presented.

Pavlovian processes and response competition as determinants of avoidance response-prevention effects ☆

Abstract Two experiments investigated the facilitation of avoidance extinction by exposure to lengthy (5-sec) shock during avoidance response prevention. In Experiment 1, animals exposed to light only or to light-shock pairings during response prevention showed equal facilitation of extinction relative to shock-only animals or to animals receiving no response prevention. Preshock rearing, directly antagonistic to the avoidance response, developed for shocked animals during response prevention and persisted during extinction for light-shock animals. Immediately before extinction, half of each group was permitted a single escape from a light-shock compound by means of the response previously required for avoidance. The only effect was upon the extinction performance of light-shock animals. Rearing was eliminated and extinction responding increased to a level far above that for any of the other animals. Experiment 2 demonstrated that the shock-only treatment affected the extinction performance and rearing of nonescape and escape animals in a manner entirely equivalent to the effects of the light-shock treatment of Experiment 1, provided stimulus conditions (light absent) were the same for all experimental phases. Thus, lengthy shock during avoidance response prevention simultaneously leads to the acquisition of competing behavior and enhances control by a warning signal or contextual stimuli over the avoidance response. Implications for the CS-only response-prevention treatment and the transfer of aversive control are discussed.

Partial control and learned helplessness in rats: Control over shock intensity prevents interference with subsequent escape

The effect upon subsequent escape acquisition of control over shock intensity in the absence of control over other shock characteristics was examined. Pretreatment involved random shocks of 1.6 and .75 mA at a density of about 10/min. The experimental group could avoid the higher shock intensity if they leverpressed at least once every 15 sec. Yoked and no-shock rats completed the triadic design. Experimental and yoked animals received all scheduled shocks. Triads were later tested for FR 2 shuttlebox escape at either the .75 mA (low) or 1.6 mA (high) intensity. During testing, avoidance rats performed as well as no-shock rats at the low intensity and escaped even more rapidly at the high intensity. Yoked rats showed interference at both intensities, with interference very marked, including many failures to escape, at the low intensity. These findings indicate that control over shock intensity, by itself, is sufficient to prevent learned helplessness and suggest that control over any salient characteristic of shock may be sufficient for immunization.

Evidence that adaptation to cold water swim-induced analgesia is a learned response

Controlling for novelty of the test context, the present experiment determined if adaptation to forced cold water swim stress-induced analgesia is learned through Pavlovian conditioning. Following baseline measurement of pain sensitivity, Group A swam in Context A for 3 min and, 8 h later, sat in Context B for 3 min. The conditions were reversed for Group B. All rats were given a tail-withdrawal test immediately after swimming or sitting in each context. On the first test day, conducted 24 h after the completion of the adaptation phase, all rats swam in Context A for 3 min, and tail-withdrawal latencies were immediately obtained after the swim. On the second test day, 24 h later, all rats swam in Context B, with tail-withdrawal latencies measured immediately thereafter. Both groups showed significantly less analgesia when tested in the adaptation context in which they previously swam than in the other context. These data provide strong evidence that adaptation to stress-induced analgesia is a learned response.

Reduction of learned helplessness by central administration of quaternary naltrexone

Prior research has established that escape impairment resulting from prior inescapable shock (IS) could be reversed by the peripheral administration of the opiate antagonist naltrexone (NTX), but not the quaternary form of naltrexone (QNTX), which when systemically administered, does not readily pass the blood-brain barrier. As it was unclear whether the failure of systemically administered QNTX to reduce shuttle escape deficits following exposure to IS could be attributed to reasons other than the restricted access of QNTX to receptor sites in the brain, rats were affixed with chronic indwelling ventricular cannulae to allow direct brain administration of QNTX. The present experiment found a significant attenuation of the escape deficit produced by prior inescapable shock following the intracerebroventricular (ICV) administration of QNTX (10 micrograms/rat). These data provide further evidence of a mediational role for central opiate receptors in the expression of escape interference following inescapable shock.

Is extinction the hallmark of operant discrimination?: Reinforcement and SΔ effects

Using a successive discrimination procedure with rats, three experiments investigated the contribution of reinforcement rate and amount of SΔ exposure on the acquisition of an operant discrimination. SD components and were always 2 min in length, while SΔ (extinction) components were either 1 min or 4 min in length; responses in SD were reinforced on one of four schedules. In Experiment 1, each of eight groups were exposed to one possible combination of rate of reinforcement and SΔ component length. At every level of reinforcement, the 4 min SΔ groups acquired the discrimination more quickly. However, within each level of reinforcement, the proportions of responding in SD as a function cumulative SΔ exposure were equivalent, regardless of the number of reinforcers earned in SD, suggesting that extinction is the “hallmark” of discrimination. Experiment 2 sought to replicate these results in a within-subjects design, and although the 4 min SΔ conditions always produced superior discriminations, the lack of discriminated responding in some conditions suggested that stimulus disparity was reduced. Experiment 3 clarified those results and extended the finding that the acquisition of operant discrimination closely parallels extinction of responding in SΔ. In sum, it appears that higher reinforcement rates and longer SΔ exposure facilitate the acquisition of discriminated operant responding.