Assessing the reviewers of animal research.
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Biomedical subjects
Publications and source records attributed to N K Dess.
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Rats selectively bred for relatively high (HiS) and relatively low (LoS) saccharin intake were offered sweet (sucrose), bitter (quinine, sucrose octaacetate), salty (sodium chloride), starchy (Polycose((R))), and sour (citric acid) solutions at several concentrations; sucrose/quinine, and sucrose/citric acid mixtures were also tested. Compared to HiS rats, LoS rats displayed weaker preferences for and lower consumption of sweet, salty, and starchy solutions. HiS and LoS rats did not differ in responses to simple bitter or sour solutions or to adulteration of sucrose with citric acid. However, quinine adulteration reduced sucrose preference more among LoS rats. Thus, selection on a saccharin intake phenotype has yielded line differences on all hedonically positive tastants and, probably as a consequence of that difference, greater finickiness specifically towards bittersweet solutions in the low saccharin-consuming line. Additional work can clarify the psychobiological mechanisms for the phenotypic difference and, potentially, the reasons for its relationship to measures of emotionality.
Whereas humans use aspartame as a sugar substitute, evidence to date from rats suggests that aspartame does not taste sweet or, more generally, hedonically positive to them. The present study provided a strong test of the appetitive properties of aspartame in rats by examining consumption of aspartame and, for comparison, several sugars by two lines of rats selectively bred for high (HiS) versus low (LoS) saccharin consumption. The HiS and LoS lines differed in consumption of fructose, glucose, sucrose, maltose, and saccharin solutions. Overall, the rats showed a weak but significant preference for aspartame. However, no line differences in aspartame consumption were observed. Thus, even among rats specifically bred on the basis of their responsiveness to sweet tastes, aspartame tastes minimally sweet or good.
Is the tongue a window to the psyche? In rats, stress alters taste, and individual differences in taste are related to measures of emotion. The present study concerned stress-induced changes in taste and its modulation by temperament in people. College students rated saccharin's bitterness and sweetness and a tone's loudness after exposure to a mild stressor. Temperament (trait arousability, pleasure, and dominance) was assessed separately. When individual differences were ignored, stress appeared to selectively increase sensitivity to saccharin's bitterness. However, the stressor's impact was modulated by temperament: Stress nonselectively augmented stimulus magnitude ratings among highly arousable individuals; relative to high-pleasure counterparts, low-pleasure individuals gave higher bitterness ratings and lower sweetness ratings after stress. Taste does seem to provide a glimpse of the emotional life of humans and other animals and opens new avenues to the study of the biological bases of affect.
Rat lines selectively bred for high ethanol consumption consume more saccharin solution than do their low-ethanol-consuming counterparts. The present study utilized the technique of reciprocal selection to examine the reliability of the saccharin/ethanol relationship; specifically, consumption of 1-10% ethanol solution was measured in rats selectively bred for high vs. low saccharin consumption (Occidental HiS and LoS lines). HiS rats consumed more ethanol than did LoS rats. These results support the idea that individual differences in ethanol and saccharin consumption share some common mechanism(s).
Exposure to inescapable shock typically reduces eating and body weight in rats. The present study examined the modulation of stress effects by prestress diet and poststress sugar availability. Maintenance on a high-fat, high-energy food attenuated stress-induced weight loss and anorexia and increased high-energy food selection when a low-energy wet mash was the only alternative. Access to sugar after stress also reduced short-term weight loss; among rats maintained on high-energy food, body weight was spared absolutely. The dependence of stress effects on pre- and poststress diet alternatives may speak to individual differences in the stress-eating relationship in humans. More generally, these results support a conceptualization of stress in terms of metabolic challenge and the integrated reorganization of energy regulatory processes.
Confirmed high saccharin (HiS)-consuming and low saccharin (LoS)-consuming rats were compared in their taste response to saccharin using a continuous intraoral infusion procedure. On 2 separate days, rats were infused with 0.1% saccharin (rate = 1 ml/min) until they rejected fluid via passive drip or forceful fluid expulsion (at which time infusion was stopped for 30 s), and then again rejected fluid within 30 s after infusion was reinitiated. Two dependent measures were collected during infusion procedures: latency to first fluid rejection and total infusion time. On the first infusion day, HiS and LoS rats produced similar latencies to first rejection and total infusion times. However, HiS rats displayed significantly longer latencies to first rejection than LoS rats on the second infusion day. The results indicate that continuous infusion procedures exposed differences between HiS and LoS lines, but only after an initial experience with saccharin, albeit a relatively short exposure. The absence of immediate line differences with infusion procedures suggests that preference differences for saccharin between HiS and LoS lines are not mediated by brainstem taste reflexes, but rather are guided by associative processes accomplished above the brainstem.
Several motivational states, such as malaise, fear, and satiety, reduce spontaneous food ingestion by rats, and differentiation of these states is often desirable. The present study used the spontaneous meal pattern to this end. The illness-inducing toxin lithium chloride delayed initiation of the first postinjection meal, and that meal was smaller and eaten more slowly (Experiments 1A and 1B). Rats exposed to tail shock also subsequently took longer to initiate meals, but meals were eaten faster and were slightly larger relative to control conditions (Experiment 2). These changes in meal patterns are different from those produced by satiety-related hormones, such as CCK or insulin, which solely reduce meal size in paradigms designed to assess physiological regulation of food intake. Taken together, these findings attest to the ability of meal patterns to distinguish malaise, fear, and satiety from one another.
The present study determined whether individual differences in neophobia during an open-field pretest predict vulnerability to inescapable electric shock, as measured by 2 tests of learned helplessness in rats. Shuttle-escape latencies and saccharin finickiness increased across groups that had received increasing numbers of inescapable shocks 24 hr earlier. Dispersion in the test measure as well as the percentage of variance explained by pretest neophobia were greater when no or few shocks were delivered in the interpolated stress phase. Pretest neophobia was positively related to stress vulnerability in both tests under these conditions. Further increments in stressor severity overwhelmed even the most stress-resistant rats, thereby decreasing dispersion in the test measure and eliminating the predictive value of pretest neophobia. This pattern of outcomes was more robust for the shuttle-escape measure of helplessness.
In most biobehavioral research using rats as subjects, saccharin is viewed as a "sugar substitute"--sweet, palatable, and conveniently lacking in calories. This characterization has merit: Saccharin seems to share some sensory, affective, and motivating properties with sugars. This paper focuses on saccharin's lesser known, aversive properties. Evidence of saccharin's distinctive taste in rats is reviewed, followed by discussion of several modulating variables. Procedures that influence rats' responses to saccharin and their measurement are summarized, and the argument is advanced that saccharin can be used to study the relationship of taste and ingestion to learning, stress, and emotional processes in rats and humans.
Rats were exposed to 100 5-s inescapable, unpredictable shocks then had access to water and saccharin or sucrose solution for 5-6 days. Shock reduced daily drinking during saccharin tests (Experiments 1, 2B, 4) and increased daily drinking during sucrose tests (Experiment 2B). In addition, shock reduced body weight when saccharin, but not when sucrose, was available (Experiments 1, 2B). The specificity of the reductions to saccharin tests (Experiments 2B, 4), equal intake of flavors shortly after stress (Experiments 2B to 4), and failure of saccharin-naive and saccharin-familiar groups to differ (Experiment 3) argue against a neophobia interpretation. Normal or above-normal drinking during sucrose (Experiment 2B) or water-only (Experiment 4) tests indicate an absence of general hedonic, motoric, or hydrational deficits. Qualitative differences in the tastes of saccharin and sucrose may underlie their disparate effects on drinking after shock. Whatever the mechanisms, the present results show that even a severe stressor can decrease or increase ingestion, depending on the flavors available.
The helplessness paradigm is used extensively in basic stress research and is an experimental model of clinical depression. In Experiment 1, exposure to unsignaled, inescapable shock resulted in finickiness about drinking a weak quinine solution, as previously reported. In contrast, exposure to escapable shock resulted in marked individual differences in finickiness that were predicted by prestress body weight. A more sensitive index of finickiness was used in Experiment 2, and a correlation between body weight and finickiness was observed in nonshocked rats. In Experiment 3, measures of quinine reactivity and body weight predicted depressive symptomatology in a nonclinical human sample. Although research in the helplessness paradigm usually focuses on environmental determinants of distress, the paradigm may help identify and explain individual differences in, or intrinsic modulation of, stress and depression.
Six experiments examined the effects of signaling the termination of inescapable shock (cessation conditioning) or shock-free periods (backward conditioning) on later escape deficits in the learned helplessness paradigm, using rats (Sprague-Dawley and Bantin-Kingman). A cessation signal prevented later performance deficits when highly variable inescapable shock durations were used during pretreatment. The inclusion of short minimum intertrial intervals during pretreatment did not alter the benefits of cessation conditioning but eliminated the protection afforded by a safety signal. The beneficial effects of both cessation and backward signals were eliminated when a single stimulus signaled shock termination and a shock-free period. Finally, a combination of cessation and backward signals was found to be most effective in immunizing against the effects of subsequent unsignaled, inescapable shock on later escape performance. These data suggest that cessation conditioning may be crucial to the prophylactic action of an escape response.
Excitatory and inhibitory classical conditioning were examined in 4-week-old, 8-week-old, and 12-week-old kittens. Conditioned respiratory suppression (CRS) was a measure of conditioned fear. The inhibitory conditioning procedure was designed to model the schedule of events that normally accompanies successful coping behavior: The safety signal predicted the cancellation of shock that would otherwise follow the danger signal, rather than simply the absence of shock. Before training, the stimuli elicited small unconditioned respiratory suppression in the 4-week-old and 8-week-old kittens, but not in the juvenile, 12-week-old kittens. During training, danger signals came to elicit robust CRS after 3-4 sessions (20-30 trials) in every age group. Acquisition of inhibition of CRS was also observed within 2-3 days (20-30 trials). The effectiveness of inhibitory stimuli improved significantly with age. The safety signal also inhibited fear (CRS) elicited by a second danger signal. Thus, the kittens learned inhibition to the safety signal per se, rather than having learned to discriminate some nonreinforced configured cue from the danger signal presented alone.
Three experiments examined food intake and body weight in rats after exposure to one session of intermittent, inescapable electric shock. Quinine adulteration and shock both suppressed feeding (Experiment 1); recovery of feeding after shock was impeded when quinine adulteration was combined with a mild daily stress reinstatement (Experiment 2). Body weight also was suppressed by shock (Experiments 1 and 2); control over shock provided some protection against this deficit (Experiment 3). These results suggest roles for "finickiness" and vulnerability to mild stressors in the maintenance of eating disorders associated with stress and depression. The findings also may have implications for interpretation of deficits in appetitively motivated behaviors after stress.
Changes in body weight and taste aversion in the learned helplessness paradigm were examined. In Experiment 1, adult male Sprague-Dawley rats drank saccharin or a control solution, followed by either 100 inescapable shocks or simple restraint. Rats were weighted daily and were tested for saccharin aversion two days after the stress session. Shocked rats gained less weight in the days after stress than restrained controls. Saccharin aversion was apparent only among rats that had consumed saccharin before the stress session. Experiment 2 examined whether control over shock affected body weight or taste aversion. Home-cage controls were included to assess the effects of restraint alone. In addition, the combined effects of shock and a toxin on aversion were studied. Rats drank saccharin solution, followed by escapable or inescapable shock, restraint, or no treatment. Then half of each group was injected with saline; the other half was injected with lithium chloride. As in Experiment 1, shock reduced body weight relative to restraint or no treatment, and shock produced a taste aversion among saline-treated rats. However, shock attenuated the aversion produced by lithium chloride, as did simple restraint. There were no differences in body weight or taste aversion between escapably and inescapably shocked rats. These results suggest a role for stress in the anorexia and weight loss associated with clinical depression and may have implications for theories of learning and learned helplessness.
The Syracuse strains of Long-Evans rats were selectively bred for good (SHA) or poor (SLA) avoidance learning in a two-way shuttle box, which resulted in a phenotypic difference that is correlated with behavior patterns indicative of emotional reactivity, SLA animals showing evidence of greater emotional reactivity than SHA animals. The first three experiments examined conditioned suppression of bar pressing and compared paired and unpaired conditioned- and unconditioned-stimulus presentations to evaluate the influence of conditioning versus primary aversive stimulation on baseline responding. SLA animals acquired conditioned suppression faster than SHA animals and also showed greater suppression of baseline responding than SHA animals. In Experiment 4, SLA animals learned a passive-avoidance task faster than SHA animals. In Experiment 5, SLA animals showed greater stress-induced suppression of drinking a weak quinine solution than SHA animals. These data are consistent with the hypothesis that SLA animals are more emotionally reactive than SHA animals.