Differentiation of escape and avoidance responding in rats.

Examined escape and avoidance performance in 144 female Holtzman albino rats by factorially arranging immediate or postponed CS and UCS termination with shuttle or bar-press escape and avoidance responses. High levels of avoidance responding occurred only when the shuttle response (running) was both the escape and avoidance response, perhaps reflecting that rats are prepared to run but contraprepared to bar press when threatened by aversive stimulation. In addition, postponed UCS termination reduced avoidance performance drastically while CS termination conditions were without effect. Measures of UCS duration and clock terminations also indicated that immediate UCS termination was superior to postponed termination but additionally showed that this was so because postponed termination seriously impaired escape behavior. Results have particular relevance for how escape responses become anticipatory. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Social behaviour in rats during escape from shock.

Following individual training in a leverpress shock escape situation, 6 pairs of male albino Wistar rats were exposed to the shock escape schedule. Escape performance of pretrained Ss deteriorated during the social session regardless of whether the pair involved a naive or 2nd pretrained S. Reliable shock-elicited fighting was observed only in pairs in which both Ss had been pretrained to escape shock, whereas no fighting occurred in paired naive Ss during exposure to the escape schedule. Disruption of individual escape performance, as well as bizarre social results (e.g., Ss making leverpressing or "holding" responses on each other), are discussed in terms of R. C. Bolles's theory of species specific defense reactions. (French summary) (19 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Retardation of extinction of an escape response by prolonged, intense goal box shock.

Studied the effects of intense, response-contingent goal box shock on the extinction of a runway-escape response in 40 male albino rats by means of a 2?×?2 factorial design in which presence vs absence of goal box shock during escape training was crossed with the same factor during extinction. Of the 2 groups trained with shock in the goal box, the 1 shocked there during extinction exhibited dramatically enhanced resistance to extinction. The group not punished there extinguished more rapidly than any of the other 4 groups. The remaining 2 groups responded at levels between these 2 groups but did not differ from each other. Results are discussed in terms of various learning-theory mechanisms, such as conditioned fear and stimulus generalization, and with emphasis on similarities between the procedures of the present study and those extant "alley-shock" and "goal-shock" self-punitive designs. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Chlordiazepoxide microinjected into the region of the dorsal raphe nucleus eliminates the interference with escape responding produced by inescapable shock whether administered before inescapable shock or escape testing.

Systemic administration of benzodiazepines before exposure to inescapable shock (IS) blocks the enhanced fear conditioning and escape learning deficits that follow exposure to IS, whereas administration before the subsequent behavioral testing eliminates the enhanced fear but not the interference with escape (N?=?44 male rats). The failure of benzodiazepines to reduce the IS-produced escape learning deficit when given before testing is inconsistent with a recent proposal that interference with escape is mediated by an IS-induced sensitization of dorsal raphe nucleus (DRN) activity. The present experiments demonstrate that chlordiazepoxide will block both the enhancement of fear and interference with escape responding when given before either IS or testing if microinjected in the region of the DRN. This suggests that systemic benzodiazepines fail to block escape deficits when given before testing because action at a site distant from the DRN counters the effect of the drug at the DRN. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Comparison of amnesias induced by electroconvulsive shock administered after training-trial footshock or noncontingent footshock in rats.

Used a 1-trial fear-conditioning paradigm in 2 experiments with 75 and 105 male Long-Evans rats, respectively. The amnesia pattern resulting from ECS delivered .5 sec after the training-trial footshock (FS/ECS) was compared with the amnesia resulting from an ECS delivered .5 sec after a noncontingent footshock (NCFS/ECS) administered 24 hrs after the training-trial footshock. FS/ECS produced a relatively strong and permanent amnesia, whereas NCFS/ECS resulted in a relatively weak and transient amnesia. Several possible explanations of these results are discussed, and it is suggested that both amnesias resulted from a disruption of memory-retrieval processes. (27 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)     

GABAA receptor activation is involved in noncontingent shock inhibition of instrumental conditioning in spinal rats.

Previous work has demonstrated that the spinal cord, isolated from higher neural structures, can support a simple form of instrumental learning. Furthermore, preexposure to uncontrollable (noncontingent) shock to the leg or tail inhibits this form of learning. The present study explores the role of GABAA receptor modulation on this inhibitory effect in spinal cord-transected rats. Intrathecal administration of the GABAA receptor antagonist bicuculline blocked induction and expression of the inhibition. The GABAA receptor agonist muscimol inhibited learning in a dose-dependent manner. However, this effect was transient and showed no additivity with shock. The findings suggest that GABAA receptor activation may work like a pharmacological switch that is activated by noncontingent shock to inhibit instrumental conditioning within the spinal cord. (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)     

Contrast effects in escape conditioning of rats.

In Exp I 39 male Holtzman albino rats ran for 20 trials from an alley where they received .2-, .4-, or .8-ma shocks to a goal box where there was no shock. All Ss were then shifted to .4 ma in the alley for 20 trials. Results show that rapid adjustment of running speeds occurred with shifts in amount of escapable shock. More importantly, however, positive and negative contrast occurred. In Exp I an experimental group (n = 10) received .2 ma on half of the trials and .4 ma on the other half, and 2 control groups (n = 10) received either .4 or .2 ma on all trials. Results show that the experimental group escaped faster on .4-ma trials than the .4-ma control group (positive contrast) and escaped more slowly on .2-ma trials than the .2-ma control (negative contrast). (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Habituation of oral responding in adult rats.

The effects of repeated oral stimulation on ingestive responding were investigated in adult rats. A series of brief intraoral infusions of flavored diet was delivered to female rats once every minute through an oral cannula. When the flavor of the infused diet remained constant, significant decreases in mouthing behavior were observed by the end of testing, whereas switching the flavor of the diet during testing resulted in enhanced responding and infusions delivered through gastric cannulas produced minimal effects. Patterns of oral responding were also similar in food-restricted rats. These patterns of responding suggest that adult rats habituate to oral stimulation. Finally, oral habituation led to decreased ingestion, whereas gastric infusions had minimal effects. Thus, oral habituation may represent a mechanism influencing intake in rats at all ages. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Suppression of responding during signaled and unsignaled shock.

The empirical basis for M. E. Seligman's (see record 1969-00554-001) safety signal hypothesis derives largely from studies of response suppression during signaled and unsignaled shock and from studies of animals' preference for signaled over unsignaled shock. Recently, the literature on preference for signaled over unsignaled shock received serious criticism, thus weakening the empirical foundations of the safety signal hypothesis. The present article reviews the literature on response suppression to determine if this, too, has been the subject of controversy and criticism. To the contrary, the suppression literature provides strong support for the safety signal hypothesis and also reports data that are compatible with much of the choice literature. This agreement between the 2 tests of the safety signal hypothesis increases confidence in the reliability of the data and the adequacy of the hypothesis. Despite this agreement, emerging data on response suppression during signaled and unsignaled shock suggest that, at best, the safety signal hypothesis emphasizes only one of the many determinants of differential response suppression. (78 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Contextual control of conditioned responding in rats with dorsal hippocampal lesions.

The control exerted by contextual cues over classically conditioned responding was assessed for rats with electrolytic lesions of the dorsal hippocampus and sham-operated controls. In 3 experiments the rats received initial training with 2 reinforced cues, each presented in its own distinctive context, followed by a nonreinforced test in which the cues were presented in the other context. Both control and operated subjects showed context specificity, as evidenced by less vigorous responding to these cues than to cues presented on test in their original contexts. The groups did not differ in their ability to learn an explicit discrimination in which a given cue was reinforced in one context and nonreinforced in a different context (although the groups did differ on a simple autoshaping task). It is concluded that a special role for the hippocampus in the contextual control of conditioned responding still remains to be demonstrated. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Behavioral responsiveness of adrenalectomized, hypophysectomized, and intact rats to electric shock.

Tested whether the altered rates of acquisition and extinction of avoidance behavior in adrenalectomized and hypophysectomized rats are associated with abnormal responsiveness to electric shock. The electrical threshold for flinch, jump, and vocalization behaviors in adrenalectomized and hypophysectomized Ss (N = 95) was measured in 2 experiments. Adrenalectomized Ss had higher thresholds for flinch and jump responses than hypophysectomized Ss, and also a higher flinch threshold than weight-matched controls. Hypophysectomized Ss had normal thresholds for all 3 behaviors. The difference in threshold for the flinch response between adrenalectomized and hypophysectomized or normal Ss was not explained by differences in body weight, although heavy Ss responded less to electric shock than light Ss. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Similarity between shock and safe areas during acquisition, transfer, and extinction of escape behavior in rats.

Demonstrated, in 3 experiments with a total of 128 female hooded rats, that performance in escape training was impaired when shock- and safe-box stimuli were similar rather than dissimilar to each other. Prior training with similar shock and safe boxes impaired responding during subsequent training or extinction under the dissimilar shock and safe condition. Prior training under the dissimilar condition did not reliably influence subsequent training or extinction under the similar shock-safe condition. Resistance to extinction under the dissimilar condition was reliably better following training with random presentations to both similar and dissimilar conditions than following training with the dissimilar condition alone. Exp III showed that impairment of escape behavior during training was attributable to response-contingent similarity between shock and safe boxes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of naltrexone and signaling inescapable electric shock on nociception and gastric lesions in rats.

Two experiments, with 144 male Long-Evans hooded rats, examined the antinociceptive effects of signaled shock and its physiological underpinnings. In Exp I, Ss were exposed to 1 of 3 shock conditions: no shock, unsignaled shock, and signaled (by a 10-sec, 1,000-Hz tone) shock. In each condition, Ss were tested hourly in the absence of tones for nociception, with vocalization to shock used as the behavioral measure. Ss receiving signaled shocks had stomach ulcer scores intermediate between those of no-shock and unsignaled shock Ss. Signaled-shock Ss also displayed a pronounced vocalization antinociception effect. This suggested that signaled shock may be less aversive. Exp II investigated a possible role of endogenous opiate peptides in these effects. Ss received hourly injections of either the opiate antagonist naltrexone (7 mg/kg, ip) or saline. There were no significant effects of naltrexone on either stomach pathology or nociception scores. The same effects of signaled shock were obtained as in Exp I. It is concluded that the role of endogenous opiates in the effects of signaled shock seen here is minimal. (38 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of d-amphetamine, pentobarbital, chlorpromazine and promazine on electric shock postponement responding by the pigeon

The effects of d-amphetamine, pentobarbital, chlorpromazine and promazine on responding under schedules of electric shock postponement were studied in pigeons. Responding was maintained by three different response-shock intervals (10, 20 and 60 seconds). Low doses (0.3-3 mg/kg) of d-amphetamine increased response rates without decreasing shock rates under all three response-shock intervals. The highest dose (10 mg/kg) of d-amphetamine increased the shock rates under all response-shock intervals and decreased the high response rate under the 10-second response-shock interval but did not decrease the lower rates of responding under the 20- and 60-second response-shock intervals. Pentobarbital decreased the high rate of responding maintained under the 10-second response-shock interval at lower dose (10 mg/kg) than the lower rates of under the 20- and 60-second response-shock intervals. The high dose (17.5 mg/kg) of pentobarbital decreased responding and the low doses (1-3 mg/kg) had no effect under all three response-shock intervals. Chlorpromazine (3-100 mg/kg) did not affect the average rate of responding under all response-shock intervals and only slightly increased shock rates under the 20- and 60-second response-shock intervals. Promazine (3-30 mg/kg) increased the rates of responding and decreased shock rates under all three response-shock intervals. Analysis of the temporal patterns of responding within the response-shock interval showed that d-amphetamine tended to induce the animals to respond earlier than they normally would in the response-shock interval while otherwise maintaining the temporal pattern of responding, pentobarbital decreased the probability of responses late in the response-shock interval, and chlorpromazine and promazine increased the probability of responses in the middle of the response-shock interval, producing a lessening of the temporal patterning of responding within the response-shock interval.     

Dissociation of interference with the speed and accuracy of escape produced by inescapable shock.

Benzodiazepines and naltrexone administered before inescapable shock block behavioral consequences of the inescapable shock such as poor shuttle box escape, reduced activity in reaction to shock, reduced social interaction, and so on. Anxiogenic β-carboline derivatives such as FR-7142 can produce these effects by themselves. In the present study, neither diazepam nor naltrexone had any effect on the interference with Y-maze choice escape accuracy produced by inescapable shock even though they both eliminated the reduction in Y-maze escape response speed produced by inescapable shock. Analogously, FG-1742 did not lead to a reduction in Y-maze choice escape response accuracy even though it did show escape responding. These data imply that inescapable shock interferes with escape choice learning and escape response speed by different mechanisms, the former not involving fear-anxiety processes. (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)     

Enhanced bradycardia induced by beta-adrenoceptor antagonists in rats pretreated with isoniazid

Recent studies indicate that the midcycle gonadotropin surge in the human occurs without an increase in hypothalamic gonadotropin-releasing hormone (GnRH) pulse frequency. In addition, previous studies employing a GnRH antagonist to provide a semiquantitative estimate of endogenous GnRH secretion suggest that the overall amount of GnRH secreted is decreased at the time of the surge. To investigate the hypothesis that a normal gonadotropin surge can be generated in the human with a decreased amount of GnRH at the midcycle, 7 GnRH-deficient subjects underwent two cycles of a physiologic regimen of intravenous pulsatile GnRH therapy. In the control cycle, 75 ng/kg/bolus of GnRH, a dose known to be sufficient for folliculogenesis, was administered throughout the cycle, using physiological frequencies. In a second cycle, the bolus dose of GnRH was decreased by one-half log order to 25 ng/kg just prior to the luteinizing hormone surge and returned to 75 ng/kg after documented ovulation. All cycles were ovulatory. The peak luteinizing hormone level (77.4 +/- 9.7 vs. 67.5 +/- 17.6 IU/l) did not differ between the control and decreased GnRH cycles. There was no difference in the peak serum estradiol level (475.8 +/- 144.1 vs. 493.2 +/- 93.0 pg/ml), follicular phase length (15.0 +/- 1.3 vs. 14.8 +/- 0.6 days), or progesterone level (22.4 +/- 5.1 vs. 34.8 +/- 5.7 ng/mg) on day 6 of the luteal phase in the control and decreased GnRH cycles, respectively. Three pregnancies were achieved in each of the control and reduced GnRH cycles. We conclude that a decreased overall amount of GnRH generates a normal midcycle gonadotropin surge and has no significant impact on luteal phase adequacy or fertility. These results provide further evidence that a decrease in endogenous hypothalamic GnRH secretion may occur at the midcycle in normal women. This study also provides evidence that the GnRH requirements for normal follicular and luteal phase dynamics may well be greater than those required for generation of a normal midcycle gonadotropin surge and ovulation in women.