Shuttle-escape Performance Research Articles

Enhancing brain adenosine signaling with the nucleoside transport blocker NBTI (S-(4-nitrobenzyl)-6-theoinosine) mimics the effects of inescapable shock on later shuttle-escape performance in rats.

Experience with unsignaled, inescapable shock represents a profound challenge to brain metabolic function and physiology. The authors have argued that behavioral impairment following this traumatic stress is a consequence of enhanced brain adenosine signaling, which promotes metabolic recovery by profoundly inhibiting neural activation. The authors tested this hypothesis by artificially increasing extracellular brain adenosine concentration by blocking uptake transport with NBTI in rats given only restraint stress in five experiments. NBTI impaired shuttle-escape performance in the manner of inescapable shock in a dose-dependent manner and acted synergistically with an ineffective number of inescapable shocks to maximally impair test performance. These deficits produced by inescapable shock and NBTI were reversed by the nonselective adenosine receptor antagonist caffeine, and the highly selective A-sub(2A) receptor antagonist CSC (8-(3-chloro-styrl)caffeine). The highly selective A-sub-1 receptor antagonist DPCPX (8-Cyclopentyl-1,3-Dipropylxanthine) failed to improve performance in rats preexposed to inescapable shock or pretreated with NBTI. These data suggest that enhanced adenosine signaling at a brain A-sub(2A) receptor impairs escape performance following inescapable shock in the learned helplessness paradigm.

Poststress glucose mitigates behavioral impairment in rats in the “learned helplessness” model of psychopathology

Three experiments examined the effects of poststress glucose treatment in the learned helplessness model of psychopathology in rats. In experiment 1, rats were given access to water or 40% aqueous glucose immediately following exposure to inescapable tailshocks or simple restraint in a 2 x 2 factorial design. Inescapably shocked rats failed to drink the glucose solution during the poststress interval and failed to show any improvement 24 hours after stress induction in shuttle-escape performance. Consequently, all rats received preexposure to a sweetened glucose cocktail in an attempt to increase poststress ingestion following inescapable shock treatment in experiment 2. Under these conditions, poststress intake of the glucose cocktail eliminated behavioral impairment in inescapably shocked rats relative to water-treated shocked rats and water- and glucose-treated restrained controls. Experiment 3 demonstrated that glucose prophylaxis occurs in the absence of sucrose when rats are preexposed to a 40% glucose solution prior to stress induction.

The effects of order of shock durations on helplessness in rats

Whereas rats exposed to a series of progressively decreasing shock durations show deficits in shuttle-escape performance 24 h later, the same number and intensity of shocks in the reverse (increasing) order of durations does not produce the “learned helplessness” effect (Balleine & Job, 1991). We conducted two experiments to establish the generality of this shock-duration order effect on other measures of distress and helplessness in rats. In Experiment 1, rats exposed to decreasing durations of inescapable shock showed reduced consumption of quinine-adulterated water (finickiness), whereas increasing durations produced no finickiness. By contrast, increasing shock durations produced greater conditioned fear to the shock context than did decreasing shock durations in Experiment 2. The differential effects of shock-duration order on finickiness and fear are explicated in terms of the specificity of fear conditioning during exposure to increasing versus decreasing series of shock duration orders.

Stress and adenosine: II. Adenosine analogs mimic the effect of inescapable shock on shuttle-escape performance in rats.

In 3 experiments, the authors examined the role of adenosine regulation in escape deficits produced by earlier exposure to inescapable shock in rats (learned helplessness). Adenosine analogs injected before escape testing mimicked the effect of earlier inescapable shock, with the magnitude of the deficit varying with dose and drug specificity for A2 adenosine receptors. Agonist-induced and stress-induced escape deficits were eliminated by pretest treatment with the centrally acting adenosine receptor antagonist theophylline but not the peripheral antagonist 8-[p-sulfophenyl]-theophylline. Finally, preexposure to an ineffective number of inescapable shocks interacted in synergy with an ineffective pretest injection of adenosine agonist to maximize deficits in escape performance. These data implicate energy regulation and a central compensatory action by adenosine in the aspects of helplessness related to conservation-withdrawal.

Stress and adenosine: II. Adenosine analogs mimic the effect of inescapable shock on shuttle-escape performance in rats.

Stress and adenosine: II. Adenosine analogs mimic the effect of inescapable shock on shuttle-escape performance in rats.

Reconsideration of the role of competing responses in demonstrations of the interference effect (learned helplessness).

In Experiment 1a, rats trained to escape shock by performing a 2-s inactive response were less impaired on a subsequent 2-way shuttle response than their yoked counterparts that received inescapable shock. In contrast, in Experiment 1b, rats trained to escape shock by performing a longer duration inactive response were more impaired on the subsequent escape task than their inescapably shocked counterparts. In Experiment 2, the results of Experiments 1a and 1b were replicated, and the inactive responses performed during pretreatment by both the escapable and inescapable shock groups were assessed and correlated with test stage 2-way shuttle escape performance. These activity data indicate that inactivity during pretreatment shock in both escapable and inescapable shock groups was a highly reliable predictor of subsequent 2-way shuttle performance, irrespective of the pretreatment shock contingency to which these Ss were exposed.

Stressor-provoked behavioral changes in six strains of mice.

Behavioral changes induced by inescapable shock were examined in six strains of mice. Exposure to shock provoked time-dependent disturbances of shuttle escape performance. In some strains the shock treatment did not affect escape performance, whereas in others profound performance deficits were evident. The inescapable shock treatment likewise induced strain-dependent alterations of performance in a forced-swim task. In most instances the shock treatment initially provoked invigorated responding, but in other strains the shock had no effect or depressed active responding. Finally, Y-maze spontaneous alteration performance was not affected by the shock treatment, although a strain-dependent increase of perseverative responses was evident. The occurrence of a stressor-induced deficit in one task in a particular strain of mouse was not predictive of behavioral alterations in a second task. These data are discussed with respect to animal models of depression and genetic differences associated with the response to stressors.

Effects of signaling inescapable shock on subsequent escape learning: Implications for theories of coping and "learned helplessness."

The present experiments reveal that shuttle-escape performance deficits are eliminated when exteroceptive cues are paired with inescapable shock. Experiment 1 indicated that, as in instrumental control, a signal following inescapable shock eliminated later escape performance deficits. Subsequent experiments revealed that both forward and backward pairings between signals and inescapable shock attenuated performance deficits. However, the data also suggest that the impact of these temporal relations may be modulated by qualitative aspects of the cues because the effects of these relations depended upon whether an increase or decrease in illumination (Experiment 2) or a compound auditory cue (Experiment 4) was used. Preliminary evidence suggests that the ability of illumination cues to block escape learning deficits may be related to their to reduce contextual fear (Experiment 3). The implications of these data for conceptions of instrumental control and the role of fear in the etiology of effects of inescapable shock exposure are discussed.

Effects of signaling inescapable shock on subsequent escape learning: Implications for theories of coping and "learned helplessness."

The present experiments reveal that shuttle-escape performance deficits are eliminated when exteroceptive cues are paired with inescapable shock. Experiment 1 indicated that, as in instrumental control, a signal following inescapable shock eliminated later escape performance deficits. Subsequent experiments revealed that both forward and backward pairings between signals and inescapable shock attenuated performance deficits. However, the data also suggest that the impact of these temporal relations may be modulated by qualitative aspects of the cues because the effects of these relations depended upon whether an increase or decrease in illumination (Experiment 2) or a compound auditory cue (Experiment 4) was used. Preliminary evidence suggests that the ability of illumination cues to block escape learning deficits may be related to their to reduce contextual fear (Experiment 3). The implications of these data for conceptions of instrumental control and the role of fear in the etiology of effects of inescapable shock exposure are discussed.

Amphetamine withdrawal: A behavioral evaluation

The effects of withdrawal from long-term amphetamine treatment on intracranial self-stimulation, forced swim-induced immobility, shuttle escape performance, acoustic startle and locomotor activity were evaluated. Mice implanted with stimulating electrodes in the lateral hypothalamus demonstrated stable and reliable rates of self-stimulation responding. After exposure to a chronic schedule of amphetamine treatment response rates were severely depressed. In addition to modifying intracranial self-stimulation responding, amphetamine withdrawal increased the duration of immobility in a forced-swim situation. Although chronic amphetamine exposure induced pronounced behavioral changes in the intracranial self-stimulation and forced swim tasks, drug withdrawal had little effect on shuttle escape performance, acoustic startle and locomotor activity. Based on these findings it was suggested that the development of post-amphetamine depression in the self-stimulation and forced swim paradigms was not related to variations in motoric or arousal mechanisms resulting from amphetamine withdrawal, but rather involved drug-induced changes in motivational processes.

Regularity of Inescapable Shock Duration Affects Behavioral Topography, but not Shuttle Escape Performance

One purpose of the present experiment was to investigate the effects of exposure to fixed and variable duration inescapable shock on the subsequent acquisition of a shuttle escape response. Another purpose was to examine closely the behavior of animals during exposure to inescapable shock in an attempt to assess directly the behavioral changes occurring during this experience. Competing response accounts of the learned helplessness effect propose the mechanism of adventitious reinforcement during inescapable shock for the learning of low activity responses. Exposure to inescapable fixed duration shock should therefore be more effective than variable duration shock of the same average value in producing subsequent escape deficits. However, the present experiment demonstrated equivalent shuttle escape deficits resulting from the two types of shock exposure. In addition, behavioral observations made during inescapable shock indicated that those behaviors immediately preceding shock offset during the first several trials were not more likely to develop than other behaviors that were virtually absent early in the session. This pattern of results does not support current competing response hypotheses, but is in agreement with learned helplessness theory.