Biomedical subjects
Publications and source records attributed to P J Bersh.
Dinsmoor (2001) rejects shock-frequency reduction as a reinforcer for avoidance behavior, and considers this to be an invalidation of so-called molar avoidance theory. This is a narrow view of operant avoidance theory, for which shock-frequency reduction is by no means the only reinforcer.
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.
Four squirrel monkeys were first exposed to a sequence of procedures that reliably generate responding maintained by brief response-contingent electric shocks arranged according to a fixed-interval schedule. After responding had become stable on the fixed-interval schedule, additional contingencies were added in tandem, whereby after completion of the interval, the spacing of responses affected shock delivery. In one procedure, responses had to be spaced more widely than their previous median value if shock were to be delivered. In the other procedure, responses had to be spaced more closely to produce shock. On the first of these procedures, decreased but stable responses rates would indicate that shock functioned as a positive reinforcer; on the second, increased response rates would indicate the positively reinforcing function. Instead, response rates accelerated on the procedure that targeted more widely spaced responses for shock delivery, and decelerated or ceased on the procedure that arranged for shocks to be produced by more closely spaced responses. Consistent with other recent findings, these results question the interpretation of performances maintained by response-contingent shock as engendered by positive reinforcement and are consistent with aversive-control interpretations. The details of that aversive control are not entirely clear, however, and these same procedures would be informative if applied to shock-maintained behavior that is generated in other ways.
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.
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.
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.
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.
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Rats were trained on a free-operant procedure in which shock duration was controlled by responses within a limited range of interresponse times. Shocks of 1.6-mA intensity occurred randomly with average density of 10 shocks per minute. As long as interresponse times were 15 seconds or less, any shocks received were at the briefer of two durations (.3 second). Whenever interresponse times exceeded 15 seconds, any shocks received were at the longer duration (1.0 second). For six of eight animals, avoidance responding developed quickly and reached levels of better than 90%. Four yoked animals stopped responding within the first few sessions. Shock duration reduction without change in shock probability or intensity was sufficient for the acquisition and maintenance of avoidance responding.
Rats were trained on a free-operant avoidance procedure in which shock intensity was controlled by interresponse time. Shocks were random at a density of about 10 shocks per minute. Shock probability was response independent. As long as interresponse times remained less than the limit in effect, any shocks received were at the lower of two intensities (0.75 mA). Whenever interresponse times exceeded the limit, any shocks received were at the higher intensity (1.6 mA). The initial limit of 15 seconds was decreased in 3-second steps to either 6 or 3 seconds. All animals lever pressed to avoid higher intensity shock. As the interresponse time limit was reduced, the response rate during the lower intensity shock and the proportion of brief interresponse times increased. Substantial warmup effects were evident, particularly at the shorter interresponse-time limits. Shock intensity reduction without change in shock probability was effective in the acquisition and maintenance of avoidance responding, as well as in differentiation of interresponse times. This research suggests limitations on the generality of a safety signal interpretation of avoidance conditioning.
Four rats were trained in darkness on a free-operant avoidance procedure in which shocks occurred randomly, but lever presses could reduce their frequency. Discrimination training followed, during which responses in light continued to reduce shock frequency, but responses in darkness had no effect. During each cycle, the light period was 4 min, while darkness lasted only until a 20-sec interval had elapsed without a response. This no-response requirement was increased to 40 sec for three animals and eventually to 60 sec for two of them. Discriminative control developed, despite a greater shock density in the dark, with response rate and number of responses per shock maintained or increasing during light and decreasing to very low values in darkness. Two animals were later exposed to a procedure in which shock density was unaffected by responding either in light or darkness. A 60-sec no-response requirement was continued in the dark. Discriminative control persisted through 42 sessions for one animal and required 45 sessions to approach extinction for the other animal. The role of the light as a potential conditioned reinforcer of other behavior in the dark was implicated in the development and persistence of discriminative control. These data support shock-frequency reduction as reinforcement for avoidance behavior.
Rats learned either a lever-press response, a shuttle response or a one-way crossing response, which produced one immediate shock but was instrumental in avoiding five identical shocks scheduled to occur later. These responses were acquired both with and without support of an escape contingency. These results support shock-frequency reduction as a sufficient condition for the acquisition and maintenance of avoidance.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.