Differences In Plasma Corticosterone Levels Research Articles

High and low feather pecking selection lines of laying hens differ in response to a judgment bias test

Feather pecking represents a serious problem in the poultry industry that can negatively affect production as well as the welfare of laying hens. Although feather pecking has been studied from many different angles, there are only a few studies of the relationship between feather pecking and cognition. This study aims to compare the cognitive performance of hens from the high feather pecking (HFP) and the low feather pecking (LFP) lines in a visual discrimination (Go/No-Go) task and to study their decision making under ambiguity using the judgment bias test.Twenty HFP and 20 LFP hens were trained in a visual discrimination task to approach a coloured feeder (white for half of the hens and black for the other half) containing a reward (one mealworm) and to refrain from approaching a feeder with a different colour (colour opposite to positive, i.e. black or white) to avoid punishment (water spraying). During the subsequent judgment bias tests hens were tested in the presence of the positive, negative or ambiguous stimulus (grey coloured feeder), always one type of stimulus at a time. The latencies to reach each of the stimuli were recorded. At the end of the visual discrimination training phase, 36 out of 40 hens successfully discriminated the positive and the negative coloured feeder. There was a slower association of the coloured feeder with the reward in the HFP line and HFP hens did not suppress the response to the negative stimulus as effective as HFP hens, which could be a sign of their high motor impulsiveness. However, in the judgment bias test HFP hens approached the ambiguous feeder significantly faster than LFP hens (HFP 13.59 ± 1.11 s, LFP 16.68 ± 1.10 s, P < 0.05), that can be interpreted as evidence that hens from the HFP line are more optimistic, i.e. that they are in a more positive affective state. The high motor impulsiveness of HFP hens provides another possible explanation for their response to the ambiguous stimulus. However, higher motor activity of the HFP line did not affect the results of the judgment bias test. Furthermore, there were no significant differences in plasma corticosterone levels between the lines, suggesting that differences in stress levels might not explain the results of the judgment bias test.

Effects of test experience, closed-arm wall color, and illumination level on behavior and plasma corticosterone response in an elevated plus maze in male C57BL/6J mice: a challenge against conventional interpretation of the test

The elevated plus maze test is a widely used test for assessing anxiety-like behavior and screening novel therapeutic agents in rodents. Previous studies have shown that a variety of internal factors and procedural variables can influence elevated plus maze behavior. Although some studies have suggested a link between behavior and plasma corticosterone levels, the relationships between them remain unclear. In this study, we investigated the effects of experience with a battery of behavioral tests, the wall color of the closed arms, and illumination level on the behavior and plasma corticosterone responses in the elevated plus maze in male C57BL/6J mice. Mice were either subjected to a series of behavioral tests, including assessments of general health and neurological function, a light/dark transition test, and an open field test, or left undisturbed until the start of the elevated plus maze test. The mice with and without test battery experience were allowed to freely explore the elevated plus maze. The other two independent groups of naïve mice were tested in mazes with closed arms with different wall colors (clear, transparent blue, white, and black) or different illumination levels (5, 100, and 800 lx). Immediately after the test, blood was collected to measure plasma corticosterone concentrations. Mice with test battery experience showed a lower percentage of open arm time and entries and, somewhat paradoxically, had lower plasma corticosterone levels than the mice with no test battery experience. Mice tested in the maze with closed arms with clear walls exhibited higher open arm exploration than mice tested in the maze with closed arms with black walls, while there were no significant differences in plasma corticosterone levels between the different wall color conditions. Illumination levels had no significant effects on any measure. Our results indicate that experience with other behavioral tests and different physical features of the maze affect elevated plus maze behaviors. Increased open arm time and entries are conventionally interpreted as decreased anxiety-like behavior, while other possible interpretations are considered: open arm exploration may reflect heightened anxiety and panic-like reaction to a novel situation under certain conditions. With the possibility of different interpretations, the present findings highlight the need to carefully consider the test conditions in designing experiments and drawing conclusions from the behavioral outcomes in the elevated plus maze test in C57BL/6J mice.

β-endorphin regulates alcohol consumption induced by exercise restriction in female mice

Animal models have long been used to study the mechanisms underlying the complex association between alcohol and stress. Female mice prevented from running on a home-cage activity wheel increase voluntary ethanol consumption. β-endorphin is an endogenous opioid involved in negatively regulating the stress response and has also been implicated in the risk for excessive drinking. The present study investigates the role of β-endorphin in moderating free-choice consumption of ethanol in response to a blocked activity wheel. Female, transgenic mice with varying levels of the opioid peptide were given daily 2-h access to 20% ethanol with rotations on a running wheel blocked on alternate days. Subjects with low β-endorphin exhibited enhanced stress sensitivity by self-administering larger quantities of ethanol on days when wheel running was prevented. β-endorphin levels did not influence voluntary activity on the running wheel. There were genotypic differences in plasma corticosterone levels as well as corticotropin-releasing hormone mRNA content in multiple brain regions associated with the stress response in these free drinking and running subjects. Susceptibility to stress is enhanced in female mice with low levels of β-endorphin, and better understanding of the role for this opioid in mitigating the response to stressors may aid in the development of interventions and treatments for excessive use of alcohol in women.

Effects of central gastrin-releasing peptide on glucose metabolism

Gastrin–releasing peptide (GRP) mediated signals in the central nervous system (CNS) influence many functions associated with energy metabolism. The purpose of the present study was to investigate the central effect of GRP on glucose metabolism in the male rat. Intracerebroventricular (icv) administration of GRP caused an immediate hyperglycaemia which was sustained till the end of the infusion. The rise in plasma glucose levels was accompanied by an increase in endogenous glucose production (EGP), as well as increases in plasma glucagon and insulin concentrations. Furthermore, no differences in plasma corticosterone levels were noted between control and GRP treated rats. These results demonstrate that central GRP increases plasma glucose levels, probably by stimulating pancreatic glucagon release and concomitantly or subsequently endogenous glucose production.

Bovine serum albumin as the dominant form of dietary protein reduces subcutaneous fat mass, plasma leptin and plasma corticosterone in high fat-fed C57/BL6J mice.

Increasing evidence suggests that the source of dietary protein can have an impact on weight gain and fat mass during high-fat feeding in both humans and rodents. The present study examined whether dietary bovine serum albumin (BSA) as the dominant source of protein alters energy balance and adiposity associated with high-fat feeding. C57/BL6J mice were given a diet with 10 % of energy from fat and 20 % of energy from casein or a diet with 45 % of energy from fat and either 20 % of energy from casein (HFD) or BSA (HFD+BSA) for 13 weeks. The HFD+BSA diet did not significantly alter daily energy expenditure, locomotor activity and RER, but did increase cumulative energy intake and percentage of lean mass while reducing feed efficiency and percentage of fat mass when compared with the HFD (P< 0·05). In subcutaneous adipose tissue (SAT), the HFD+BSA diet increased the mRNA levels of PPARα (PPARA), carnitine palmitoyltransferase 1b (CPT1b) and uncoupling protein 3 (UCP3), but reduced the mRNA level of leptin when compared with the HFD (P< 0·05). The SAT mRNA levels of PPARA, CPT1b and UCP3 were negatively correlated (P< 0·05) with SAT mass, which was reduced in HFD+BSA mice compared with HFD controls (P< 0·01). No differences in epididymal fat mass existed between the groups. The HFD+BSA diet normalised plasma leptin and corticosterone levels compared with the HFD (P< 0·05). While differences in leptin levels were associated with the percentage of fat mass (P< 0·01), changes in corticosterone concentrations were independent of the percentage of fat mass (P< 0·05). The data suggest that the HFD+BSA diet influences plasma leptin levels via SAT mass reduction where mRNA levels of genes linked to β-oxidation were increased, whereas differences in plasma corticosterone levels were not related to fat mass reduction.

Preferential loss of dorsal-hippocampus synapses underlies memory impairments provoked by short, multimodal stress

The cognitive effects of stress are profound, yet it is unknown if the consequences of concurrent multiple stresses on learning and memory differ from those of a single stress of equal intensity and duration. We compared the effects on hippocampus-dependent memory of concurrent, hours-long light, loud noise, jostling and restraint (multimodal stress) with those of restraint or of loud noise alone. We then examined if differences in memory impairment following these two stress types might derive from their differential impact on hippocampal synapses, distinguishing dorsal and ventral hippocampus. Mice exposed to hours-long restraint or loud noise were modestly or minimally impaired in novel object recognition, whereas similar-duration multimodal stress provoked severe deficits. Differences in memory were not explained by differences in plasma corticosterone levels or numbers of Fos-labeled neurons in stress-sensitive hypothalamic neurons. However, although synapses in hippocampal CA3 were impacted by both restraint and multimodal stress, multimodal stress alone reduced synapse numbers severely in dorsal CA1, a region crucial for hippocampus-dependent memory. Ventral CA1 synapses were not significantly affected by either stress modality. Probing the basis of the preferential loss of dorsal synapses after multimodal stress, we found differential patterns of neuronal activation by the two stress types. Cross-correlation matrices, reflecting functional connectivity among activated regions, demonstrated that multimodal stress reduced hippocampal correlations with septum and thalamus and increased correlations with amygdala and BST. Thus, despite similar effects on plasma corticosterone and on hypothalamic stress-sensitive cells, multimodal and restraint stress differ in their activation of brain networks and in their impact on hippocampal synapses. Both of these processes might contribute to amplified memory impairments following short, multimodal stress.

The influence of crate height on selected biochemical indices in captive‐reared mallards

The aim of this study was to investigate the effects of crate type (particularly its height) on selected biochemical indices in captive-reared mallards (Anas platyrhynchos). The physiological changes in response to 2-h crating in crates of either 20 cm or 26 cm height were monitored in 6-week-old mallards. Plasma corticosterone concentrations showed an increase (P = 0.036) in mallards crated in crates of 26 cm height in comparison with control non-crated birds, whereas no difference in plasma corticosterone levels was found between mallards crated in crates of 20 cm height and control non-crated birds. Lower concentrations of plasma triglycerides (P < 0.05) and uric acid (P < 0.05) were found in crated mallards in comparison with control non-crated birds; the height of the crates had no effect. Mallards crated in crates of 26 cm height also exhibited a higher (P = 0.032) plasma lactate dehydrogenase concentration in comparison with control non-crated birds, whereas no difference (P > 0.05) was found in lactate dehydrogenase concentrations in mallards crated in crates of 20 cm height. Our results suggest that crating mallards in lower crates (20 cm) may be less stressful than keeping them in crates allowing vertical movements of the birds.

Effects of repeated tickling on conditioned fear and hormonal responses in socially isolated rats

Positive emotional states have been reported to modify human resilience to fear and anxiety, but few animal models are available to elucidate underlying mechanisms. In the current study, we examined whether 2 weeks of tickling, which is considered to evoke positive emotions, alters conditioned fear and hormonal reactions in Fischer rats. We conditioned rats to fear an auditory tone which was initially paired with a mild foot-shock (0.2mA), and retention test was conducted 48h and 96h after conditioning. During these tests, we found that prior tickling treatment significantly diminished fear-induced freezing. To examine the effects of tickling on sympatho-adrenal and hypothalamic-pituitary-adrenal responses associated with conditioned fear, we measured plasma catecholamine and corticosterone levels in the retention test 96h after conditioning. The plasma catecholamine concentration of non-tickled rats was higher than basal levels, whereas tickled rats showed significantly reduced concentrations of both plasma adrenaline and noradrenaline. No significant differences in plasma corticosterone levels were observed between tickled and non-tickled rats. These results suggest that repeated exposure to tickling can modulate fear-related behavior and sympatho-adrenal stress responses.

Different emotional disturbances in two experimental models of temporal lobe epilepsy in rats.

Affective symptoms such as anxiety and depression are frequently observed in patients with epilepsy. The mechanisms of comorbidity of epilepsy and affective disorders, however, remain unclear. Diverse models are traditionally used in epilepsy research, including the status epilepticus (SE) model in rats, which are aimed at generating chronic epileptic animals; however, the implications of different SE models and rat strains in emotional behaviors has not been reported. To address this issue, we examined the emotional sequelae of two SE models of temporal lobe epilepsy (TLE) – the lithium-pilocarpine (LIP) model and the kainic acid (KA) model – in two different rat strains (Wistar and Sprague-Dawley), which differ significantly in the pattern and extent of TLE-associated brain lesions. We found differences between LIP- and KA-treated animals in tests for depression-like and anxiety-like behaviors, as well as differences in plasma corticosterone levels. Whereas only LIP-treated rats displayed increased motivation to consume saccharin, both SE models led to reduced motivation for social contact, with LIP-treated animals being particularly affected. Evaluation of behavior in the open field test indicated very low levels of anxiety in LIP-treated rats and a mild decrease in KA-treated rats compared to controls. After exposure to a battery of behavioral tests, plasma corticosterone levels were increased only in LIP-treated animals. This hyperactivity in the hypothalamus-pituitary-adrenocortical (HPA) axis was highly correlated with performance in the open field test and the social interaction test, suggesting that comorbidity of epilepsy and emotional behaviors might also be related to other factors such as HPA axis function. Our results indicate that altered emotional behaviors are not inherent to the epileptic condition in experimental TLE; instead, they likely reflect alterations in anxiety levels related to model-dependent dysregulation of the HPA axis.

Individual differences in cocaine-induced locomotor activity of male Sprague–Dawley rats are not explained by plasma corticosterone levels

Humans differ in their initial response to, and subsequent abuse of, addictive drugs like cocaine. Rodents also exhibit marked individual differences in responsiveness to cocaine. Previously, we classified male Sprague–Dawley rats as either low or high cocaine responders (LCRs or HCRs, respectively), based on their acute low-dose cocaine-induced locomotor activity, and found that with repeated drug exposure LCRs exhibit greater cocaine locomotor sensitization, reward and reinforcement than HCRs. Differential cocaine-induced increases in striatal dopamine help to explain the LCR/HCR phenotypes. Differential levels of stress and/or anxiety could also contribute but have not been explored. Here we measured open-field activity and plasma corticosterone levels both pre- and post-cocaine treatment in LCRs, HCRs, and saline-treated controls. The three groups did not differ in baseline locomotor activity or corticosterone levels. Importantly, LCR/HCR differences in corticosterone levels were also not observed following acute cocaine (10 mg/kg, i.p.), when cocaine induced approximately 3.5-fold greater locomotor activity in HCRs than LCRs. Additionally, there were no LCR/HCR differences in plasma corticosterone levels following 5 days of once-daily cocaine, during which time LCRs developed locomotor sensitization such that their cocaine-induced locomotor activity no longer differed from that of HCRs. Likewise, there were no group activity differences in any of four concentric zones within the open-field chamber. In summary, neither plasma corticosterone levels nor thigmotaxis-type anxiety appears to be a factor that contributes to the observed cocaine-induced LCR/HCR behavioral differences.

Is hyper-aggressiveness associated with physiological hypoarousal? A comparative study on mouse lines selected for high and low aggressiveness

Aggressiveness is often considered a life-long, persistent personality trait and is therefore expected to have a consistent neurobiological basis. Recent meta-analyses on physiological correlates of aggression and violence suggest that certain aggression-related psychopathologies are associated with low functioning of the hypothalamo-pituitary-adrenal (HPA) axis and autonomic nervous system (ANS). We tested this hypothesis in mice selected for high and low aggressiveness by measuring baseline plasma corticosterone levels and, via radiotelemetry, heart rate and core body temperature. The radiotelemetric recordings were made for 48 h under baseline undisturbed conditions and for 90 min after a handling stressor. Consistent with the hypoarousal hypothesis of violence, we found lower resting heart rates in two out of the three highly aggressive selection lines. In contrast, body temperature during the active phase, as another ANS-regulated physiological parameter, was higher in two out of three highly aggressive lines. The handling-induced tachycardiac and hyperthermic responses were similar across the six mouse lines except for the most docile and obese line, which showed a blunted reactivity. Besides significant differences between strains, no differences in plasma corticosterone levels were found between the high- and low-aggressive phenotypes. These results are discussed in relation to the different types of aggression (normal versus pathological) exhibited by the three highly aggressive lines. We conclude that while high trait-like aggressiveness is generally associated with a higher active phase core body temperature, only animals that express pathological forms of aggression are characterized by a low resting heart rate.

Age, sex and early environment contribute to individual differences in nicotine/acetaldehyde-induced behavioral and endocrine responses in rats

Neonatal handling was used to evaluate the influence of early environment on responses to nicotine. Rats exposed as pups to daily short-term separation from the dam (H) were compared to non-handled (NH) controls. In experiment 1, prepubescent males and females, aged postnatal day (P) 30, were tested for the effect of nicotine/acetaldehyde (NicAc) on open field behavior and plasma corticosterone levels. NicAc induced increases in ambulatory activity and time spent in the center of the field in NH, but not H, males. Drug-induced increases in initial ambulatory activity, but not center time, were also seen in NH and H females. Handling, but not sex, contributed to group differences in plasma corticosterone levels. In experiment 2, NH and H rats were tested for acquisition of NicAc self-administration at three ages, P27–31, P34–38 and P90–94. Age and sex, but not handling, contributed to differences in performance of this task. Whereas males exhibited a decrease in responding with age, females did not. These findings demonstrate that neonatal handling may serve as an experimental model for individual differences in sensitivity to tobacco constituents. Furthermore, the current study indicates that stress reactivity, age and sex may play differential roles in initiating smoking behavior.

Attenuated corticosterone response to chronic ACTH stimulation in hepatic lipase-deficient mice: evidence for a role for hepatic lipase in adrenal physiology

Hepatic lipase (HL), a liver-expressed lipolytic enzyme, hydrolyzes triglycerides and phospholipids in lipoproteins and promotes cholesterol delivery through receptor-mediated whole particle and selective cholesterol uptake. HL activity also occurs in the adrenal glands, which utilize lipoprotein cholesterol to synthesize glucocorticoids in response to pituitary ACTH. It is likely that the role of adrenal HL is to facilitate delivery of exogenous cholesterol for glucocorticoid synthesis. On this basis, we hypothesized that HL deficiency would blunt the glucocorticoid response to ACTH. Furthermore, because exogenous cholesterol also is derived from the LDL receptor (LDLR) pathway, we hypothesized that LDLR deficiency would blunt the response to ACTH. To test these hypotheses, we compared the corticosterone response to eight daily ACTH injections in HL-deficient (hl-/-), LDLR-deficient (Ldlr-/-), and HL- and LDLR-doubly deficient (Ldlr-/- hl-/-) mice with that in wild-type (WT) mice. Plasma corticosterone levels were measured on days 2, 5, and 8. Differences in plasma corticosterone levels between genotypes were analyzed by Kruskal-Wallis one-way ANOVA on ranks and pairwise multiple comparisons by Dunn's test. Our results demonstrate a trend toward reductions in plasma corticosterone levels on day 2 and significant reductions on day 5 and day 8 in the knockout models. Thus, on day 5, plasma corticosterone levels were reduced by 57, 70, and 73% (all P < 0.05) and on day 8 by 76, 59, and 63% (all P < 0.05) in hl-/-, Ldlr-/-, and Ldlr-/- hl-/- mice, respectively. These results demonstrate that HL deficiency, like LDLR deficiency, blunts the adrenal response to chronic ACTH stimulation and suggest a novel role for HL in adrenal physiology.

Adrenocorticotropin Stress Response but Not Glucocorticoid-Negative Feedback Is Altered by Prenatal Morphine Exposure in Adult Male Rats

The present study was designed to investigate the effects of prenatal morphine exposure on the hypothalamic-pituitary-adrenal (HPA) axis-regulated stress responses by measuring restraint stress-induced changes in the adrenocorticotropic hormone (ACTH) and corticosterone (CORT) levels. In experiment 1, plasma levels of ACTH and CORT in prenatally morphine-, saline-exposed and control male rats were determined before and at several times after restraint stress. There were no statistically significant differences in plasma ACTH and CORT levels before restraint stress between the groups. However, prenatal morphine exposure dampened the stress-induced increase and spontaneous recovery of ACTH levels after the restraint stress. There were no differences in plasma CORT levels between the three groups either before or at any time after restraint stress. Experiment 2 was designed to investigate the sensitivity of negative feedback of glucocorticoids using the dexamethasone (DEX) suppression test. DEX was administered at different doses (0.001, 0.01, 0.1 and 1.0 mg/kg) and ACTH and CORT plasma levels were measured before and at several times after restraint stress in prenatally morphine- and saline-exposed males. DEX pretreatment eliminated the differences observed in ACTH responses to stress in morphine- and saline-exposed males. DEX pretreatment dose dependently suppressed the restraint stress-induced increased plasma ACTH concentration. In plasma CORT levels, DEX pretreatment dose dependently suppressed the restraint stress-induced increased plasma CORT concentration regardless of prenatal drug exposure. Thus, the present study demonstrates that prenatal morphine exposure alters the ACTH and CORT responses to stress but not the sensitivity of negative feedback of glucocorticoids.

Serotonin depletion does not alter lipopolysaccharide-induced activation of the rat paraventricular nucleus.

We have investigated the effects of serotonin depletion on immune-mediated activation of the hypothalamo-pituitary-adrenal (HPA) axis. Corticotrophin-releasing factor (CRF) mRNA, c-fos mRNA and Fos peptide responses in the paraventricular nucleus (PVN) together with circulating levels of corticosterone were assessed in response to i.p. injections of three doses of lipopolysaccharide (LPS) both in control animals and animals pretreated with p-chlorophenylalanine (PCPA). Conscious animals received either an i.p. injection of 0.5 ml saline or 200 mg/kg PCPA in 0.5 ml saline on 2 consecutive days. This treatment resulted in a 93% depletion of serotonin on the fourth day. On day 4, animals received i.p. injections of LPS (2.5 mg/0.5 ml saline, 250 micrograms/0.5 ml or 50 micrograms/0.5 ml; E. coli 055:B5), or saline injections as controls. Pretreatment with PCPA had no effect on the basal levels of corticosterone, or on the elevated levels induced by the three doses, of LPS. Fos peptide and c-fos mRNA were undetectable in control animals, and Fos-like immunoreactivity increased in a dose-dependent manner following i.p. LPS in both control and PCPA-pretreated animals. C-fos mRNA expression induced by LPS was unaffected by serotonin depletion. Following the lowest dose of LPS, CRF mRNA did not change above control levels, however, the medium and high doses of LPS produced a significant (P < 0.05) increase in CRF mRNA levels in both depleted and intact animals. To confirm the temporal effects of serotonin depletion on activation of the HPA axis we collected plasma at 30 min, 1, 2, 3, 4, 5, and 6 h after LPS in both intact and serotonin-depleted animals. No significant differences in plasma corticosterone levels were found at any of the time points between intact and depleted animals. It appears that, at least under these experimental conditions, serotonergic inputs do not seem to play a major role in mediating the effects of LPS on changes in mRNA levels in the PVN or on the subsequent activation of the HPA axis.

Energetic constraints and steroid hormone correlates of male calling behaviour in the túngara frog

We investigated physiological constraints on calling behaviour in the túgara frog, Physalaemus pustulosus. First, we examined the hypothesis that energetic factors limit calling. Time spent in chorus activity is the best predictor of male mating success (Ryan, 1985). Manipulation of food availability demonstrated that males given supplemental food were more likely to call than males without supplemental food. Males without supplemental food were less likely to call even though their lipid reserves were only slightly less than males given the supplemental food, suggesting that part of the increased energy obtained from the supplemental food may have been channelled into calling to attract females. Secondly, we examined the role of steroid hormones in switching between reproductive and non‐reproductive behaviours. Calling males had higher levels of plasma testosterone than silent males. Experimental elevation of corticosterone decreased testosterone levels and the likelihood of calling, thus linking both of these steroid hormones to calling behaviour. Males who responded to supplemental food by increasing calling had higher levels of testosterone than those without supplemental food, but there was no difference in plasma corticosterone levels. Overall, the results suggest that energetic factors affect calling behaviour and that one potential mechanism for this affect is through plasma testosterone levels. Corticosterone can decrease calling behaviour, however, corticosterone does not appear to mediate the effect of energetic factors on calling behaviour. These data are consistent with the hypothesis that energetic factors ultimately constrain sexual selection for calling behaviour.

Inescapable shock induces the opposite changes of the plus-maze test behavior in rats with divergent coping strategy

Behavior in the elevated plus-maze and plasma corticosterone levels were investigated in Koltushi high-avoidance (KHA) and low-avoidance (KLA) rat strains subjected to inescapable shock (IS) or daily handling for 10 days. These strains have been genetically selected on the basis of divergent acquisition of a conditioned avoidance response in a two-way shuttle-box. Naive KHA rats were more anxious than KLA ones. Following exposure to IS, the time spent in open arms was increased in KHA rats but decreased in KLA rats. After handling, the time spent in open arms increased only in KHA rats and became similar in both strains. There were no differences in plasma corticosterone levels between naive animals. Exposure to either IS or handling increased the plasma corticosterone levels in KLA rats. In KHA rats, handling reduced the plasma corticosterone levels, and exposure to IS had no effect. The present results suggest that the stress-induced changes in anxiety levels depend on the coping strategy of the subject.

The dexamethasone suppression test in genetically different rats exposed to inescapable and escapable electric shocks

The Dexamethasone Suppression Test (DST) was applied to male rats of Koltushi high- (KHA) and low-avoidance (KLA) strains, genetically selected on the basis of divergent acquisition of a conditioned avoidance response in a two-way shuttlebox. Rats were exposed to either inescapable (IS) or escapable (ES) electroshock. IS produced escape deficit in a shuttle box only in KHA rats. ES enhanced escape failures only in KLA rats. There were no differences in plasma corticosterone levels between naive KLA and KHA rats. IS led to increase of the post-dexamethasone corticosterone levels in KHA rats, while both basal and stress-induced corticosterone levels in the KHA strain remained unchanged following IS. In KLA rats exposed to IS, both pre- and post-dexamethasone basal corticosterone levels were increased and stress-induced cortisterone levels were decreased. Thus, resistance to the DST after IS occurred only in KHA rats. ES led to enhanced basal and reduced stress-induced corticosterone levels in KLA rats compared to KHA rats before and after dexamethasone treatment. These findings suggest that the HPA axis reactivity following aversive stimuli depends on the interaction between genotype and stressor controllability.

Genetic differences in plasma corticosterone levels in response to nicotine injection

Changes in plasma corticosterone (CCS) levels following intraperitoneal injections of nicotine were measured in four inbred mouse strains: DBA/2Ibg, C57BL/6Ibg, C3H/2Ibg, and A/J. In all four strains, nicotine produced a dose-dependent (0.5–2.0 mg/kg nicotine) increase in plasma CCS levels which peaked 10–30 min after injection. Saline increased plasma CCS levels in C57BL, A, and C3H, but not in DBA mice. After correcting for plasma CCS levels produced by saline injection, the nicotine-induced rise in plasma CCS was significantly lower for the C57BL strain than for the other three strains tested. These mouse strains also varied in their responses to saline injection with the rank order: C57BL > A = C3H > DBA. However, the two most divergent strains (C57BL and DBA) did not differ in the effects of a cold water stress. The response to nicotine was completely inhibited by mecamylamine in two strains tested (C3H and C57BL) whereas the response to saline injection was unaffected, suggesting that only the response to nicotine was mediated by nicotinic receptors. It is clear that elevations in plasma CCS induced either by saline injection or by nicotine are influenced by genetic factors.

Predictability, control, and the pituitary-adrenal response in rats.

Five experiments were performed to compare to effects of signaled and unsignaled shock on the pituitary-adrenal response of rats. In Experimental 1, exposure to the two procedures yielded no difference in plasma corticosterone levels. In Experiment 2, the addition of a food-reinforced lever-pressing baseline produced conditioned suppression in the signaled condition but bo group difference in steroid values. In Experiment 3, in order to guard against steroid elevations produced by exposure to shock per se, blood samples were obtained during brief test sessions prior to the occurrence of shock. The procedure resulted in a significant elevation in the steroid levels of the signaled shock group. In Experiment 4, a within-subjects sampling procedure revealed that disparate group steroid values obtained earlier in the session had converged by the end of the test session. The final experiment replicated the original failure to obtain a steroid difference due to predictability in the absence of a behavioral baseline, despite the fact that blood samples were obtained by using the early "probe" sampling procedure. Collectively, these results suggest that (a) the effects of predictability are largely seen in the temporal pattern of steroid elevation and not in their terminal values, (b) the effects of predictability on steroids are modulated by the availability of control, and (c) control is not confined to the stimulus that is being predicted.