Integrative physiological and behavioral science : the official journal of the Pavlovian Society最新文献

The purpose of this study was to develop a laboratory animal model of human shift work. Two methods of monitoring circadian rhythms in rats were employed: an activity wheel cage, where number of wheel revolutions (WR) were counted, and an internal radio transmitter, which recorded gross motor activity (GMA) and body temperature (BT). Rats were implanted with biotelemetry transmitters that detected GMA and BT and were placed in activity wheel cages. A 12 hour/12 hour light/dark cycle was maintained. Subjects were subdivided into two groups: control and experimental. Following a habituation period of 15 days, in which animals had ad-libitum access to food and water and unlimited access to the running wheel, the experimental period ensued for 22 days. Control animals were food restricted and their activity wheels were locked during the light; experimental animals were food restricted and their activity wheels were locked during the dark. At the end of the experimental period, animals were returned to the habituation paradigm for 15 days. Recordings of WR, GMA and BT, as well as daily monitoring of body weight and food intake, indicated that experimental animals resembled humans employed in a shift work schedule. In the experiment, the light entrainable oscillator and the food entrainable oscillator were uncoupled in experimental animals, producing alterations in activity/rest cycles, consummatory behavior, and overt behavior. Since similar alterations occur in shift workers, it is proposed that the experimental paradigm presented in this manuscript is a useful model of shift work and provides a framework upon which future experiments may be conducted.

A study was conducted to expand the conventional view of cardiovascular (CV) reactivity by using the idiodynamic paradigm for investigation of individuals. Patterns of autonomic CV regulation were assessed in six subjects across diverse laboratory tasks on three separate occasions. Individual CV profiles were derived from these data with P-technique factor analysis, and then group aggregated with chain P-technique. The composite pattern suggested a three-component solution consisting of cardiac rate, cardiac contractility, and peripheral resistance factors. Individual profiles were compared to the composite pattern; these profiles differed in the number of components derived, percentage variance explained by these components, and relative dominance of specific CV components. A hypothesis that emerged is that the subjects differed in the complexity of CV control. It appears that the idiodynamic framework, combined with novel research designs and statistical methods, may help expand the view of CV reactivity beyond the traditional unitary view as response magnitude.

The basolateral amygdaloid complex (BLA) and orbitofrontal cortex (OFC) share extensive reciprocal connections, and interactions between these regions likely contribute to both mnemonic and affective processes. The present study examined the potential differential contributions of the BLA and OFC to performance of an olfactory discrimination task that incorporates auditory conditioned reinforcement and to expression of immediate post-shock freezing behavior. Damage to the BLA had little effect on performance of the conditioned reinforcement task but abolished immediate post-shock freezing behavior. In contrast, damage to OFC resulted in both a mild but significant performance decrement in the conditioned reinforcement task and a significant attenuation of immediate post-shock freezing behavior. These findings suggest that immediate post-shock freezing behavior is likely critically dependent upon interactions between the BLA and OFC. However, although mnemonic processes underlying accurate performance of the conditioned reinforcement task might be supported by OFC in part, such processes are independent of either the BLA or interactions between these two regions.

Exposure to inescapable stressors enhances cue-dependent learning in male rats; enhanced learning is apparent as facilitated acquisition of the classically conditioned eyeblink respouse (CCER). The proinflammatory cytokines, in particular interleukin (IL)-1beta, are presumed to orchestrate a number of acute-phase stress responses in rats, most notably fever, reduced feeding, and inactivity. Little is known of the impact proinflammatory cytokines have on learning and memory processes. Here, we address the effects of IL-1beta treatment on acquisition of the classically conditioned eyeblink response 2 hours [?] after injection in male rats. Training was accomplished with a delay-type paradigm (500-ms conditional stimulus coterminating with a 10-ms periorbital unconditional stimulation). Facilitated acquisition was clearly apparent in rats treated with IL-1beta (3.0 microg/kg). In a second experiment, we compared rats treated with 3.0 microg/kg to those treated with 1.0 microg/kg. Facilitated acquisition was reproduced, but the lower dose did not appreciably affect acquisition. These data further support contentions that IL-1beta has anxiogenic properties, affecting basic new motor learning in a manner similar to that observed after exposure to stress.

Several recent studies have investigated relationships between post-traumatic stress disorder (PTSD) and learning and memory problems. These reports have found in general that not only does PTSD affect trauma-related memories, but when patients with PTSD are compared with similar trauma patients without PTSD, general memory impairments have been found. The present paper reports a study in which associative learning, using Pavlovian eyeblink conditioning, was investigated in combat veterans with and without chronic PTSD, using interstimulus intervals of 500 and 1000 msec in two separate experiments. Although several recent reports suggest that larger-magnitude autonomic conditioned responses occur in patients with PTSD during Pavlovian conditioning, the present study found evidence of impaired Pavlovian eyeblink conditioning in combat veterans with and without PTSD, compared to non-combat veterans. Although these data suggest that combat leads to an impaired associative learning process regardless of whether PTSD is apparent, a group of community-dwelling combat veterans not under medical treatment showed normal conditioning, suggesting that variables other than prior combat must also be involved.

This paper reviews recent findings from our laboratories concerning metabolic and immune mediators of behavioral depression in rats. Specifically, a single injection of 6 mg/kg of reserpine substantially increases behavioral depression, as evidenced by an increase in the amount of time spent floating by independent groups of rats tested for swim performance at various times during the next week. The behavioral impairment consists of two components. An early component emerges one hour after reserpine treatment and persists for about 24 hours. The deficit is not reversed by intracranial ventricular infusion of the receptor antagonist for interleukin-1beta (IL-1beta). A second, late-component deficit appears approximately 48 hours after reserpine treatment and recovers within a week. Late-component depression is reversed by central infusion of the IL-1beta receptor antagonist, and is mimicked by central infusion of the proinflammatory cytokine. Importantly, both early and late components of reserpine-induced depression and IL-1beta induced depression are reversed by a systemic injection of the highly selective A2A adenosine receptor antagonist 8-(3-Chlorostyryl) caffeine. These data are discussed in terms of the overlap in the conservation-withdrawal reaction during sickness, traumatic stress, and major depression and the regional contribution of purines and cytokines to the organization of this reaction in the brain.

The two experiments reported examine the role of temporal contiguity on judgments of contingency in a human analogue of the Pavlovian task. The data show that the effect of the actual delay on contingency judgment depends on the observer's expectation regarding the delay. For a fixed contingency between the cue and the outcome, ratings of the contingency are higher when the actual delay is congruent with the observer's expectation than when it is incongruent. We argue that our data can be understood within the context of the temporal coding hypothesis.

Conditioned taste aversion (CTA) learning is an adaptive, robust, well-established learning and memory paradigm. Strong taste aversions develop to the conditioned stimulus (CS = saccharin) despite long delays between exposure to the CS and unconditioned stimulus (US = LiCl). Rats display a sexually dimorphic pattern of long-delay CTA learning (Foy et al., 1996). The present study examines whether this sex difference is a result of activational or organizational hormone action, because here we implanted gonadectomized rats with their normal hormone replacements, or with opposing hormones prior to testing in a 4-hr delayed CTA learning task. We found that gonadally intact male rats displayed a more robust CTA response than intact female rats. Gonadectomy essentially eliminated this sex difference; gonadectomized males and gonadectomized females displayed similar CTA responses. In gonadectomized rats, when their normal sex hormones were replaced with implanted hormone pellets, the sex difference in CTA learning was reinstated. In contrast, when gonadectomized rats were implanted with opposing hormones, the sex difference was reversed. Gonadectomized female rats implanted with 5alpha-DHT pellets (metabolite of testosterone) displayed a stronger CTA response compared to gonadectomized males implanted with 17beta-estradiol pellets. Regardless of the original developmental hormonal environment, our study suggests that an activational manipulation of circulating hormones serves to significantly influence long-delay CTA learning in rats.

Many studies have alluded to sexually dimorphic changes in behavior following stress. Although many have suggested that these changes are a function of stress-induced changes in learning and memory, there are questions regarding whether performance in those learning and memory tasks are influenced by stress-induced changes in drive more than in actual learning and memory processes. We used the classically conditioned eyeblink response (CCER) to determine whether slowed learning following stress in females can be explained by changes in unconditional response (UR) amplitude, a sign of a stress-induced shift in sensory reactivity. In addition, we had a second treatment group injected with the pro-inflammatory cytokine IL-1beta to serve as an interoceptive stress condition, a physiological stressor with minimal stimulation to the animal. Replicating the work by Shors and colleagues, we found that stressed female rats had slower acquisition of the conditioned response (CR), but we also found that an IL-1beta injection leads to a slowing of CR acquisition. However, in both cases, UR amplitude was lower in the treatment groups. We followed up these results by testing sensory reactivity through the acoustic startle response (ASR), where the magnitude of the ASR was marginally, but nonsignificantly, reduced by the same dose regimen of IL-1beta. Together, these experiments suggest that tailshock stress and immune signaling (IL-1beta) reduce sensory reactivity and the saliency of the stimuli used in the CCER, leading to slower learning in female rats.

Studies regarding extinction and spontaneous recovery of the discriminative stimulus effects of drugs are limited. Eight rats were initially trained to discriminate nicotine (0.4 mg/kg) vs. ethanol (800 mg/kg). For four rats, itraperitaneal (IP) administrations of nicotine fifteen minutes prior to fifteen-minute training sessions served as a discriminative stimulus (SD) for predicting food-reinforced lever pressing (VI-1 min). On other sessions ethanol functioned in predicting nonreinforcement (SA). The stimulus roles of the drugs were counterbalanced for the remaining four rats. SA and SD sessions alternated quasi-randomly with two daily sessions at 1000 and 1400 hours. Discriminative control was not disrupted following ten extinction sessions under a non-drug/saline condition, but was disrupted following extinction sessions under the original training drugs. Instances of spontaneous recovery (SR) occurred throughout extinction under the drug condtions. There was no evidence for SR two weeks following extinction, but partial recovery four weeks following the final extinction phase. Contextual status (context renewal) had neither a restorative or disruptive impact on extinguished or discriminated responding, respectively. These results support and extend the limited number of other studies by demonstrating extinction and spontaneous recovery of responding discriminated by two distinct drugs. Some theoretical interpretations regarding history effects and training in the context of drug discrimination are entertained.