Endocannabinoid signaling as an intrinsic component of the circuits mediating adaptive responses to repeated stress exposure in adult male sprague dawley rats.

Evidence implicates the endocannabinoid (eCB) system as a negative modulator of neural and endocrine responses to acute stressors. Recently, eCB signaling was also reported to contribute to habituation of hypothalamo-pituitary-adrenal (HPA) axis responses to repeated homotypic stress. The present studies were initiated to distinguish a potential role of eCB signaling in the expression vs. the acquisition of habituation of the HPA axis response to repeated stress. In each of three experiments, adult male Sprague Dawley rats were exposed to daily, 30-minute sessions of loud white noise (95 dB), which resulted in a progressive decrease in HPA axis response over successive days. Cannabinoid receptor 1 (CB1) antagonist AM251 (0.5, 1.0 or 2.0 mg/kg, i.p.) was used to examine the role of eCB signaling in homotypic stressor habituation and heterotypic (novel) stressor cross-sensitization of neuroendocrine activity. Pretreatment with high dose (2.0 mg/kg) AM251 before each of 7 consecutive, daily loud noise exposures (acquisition of habituation) resulted in potentiation of stress-induced HPA axis activation and disruption of habituation. After an 8th loud noise exposure without AM251 pretreatment, the same group of rats displayed a habituated plasma corticosterone (CORT) level similar to that of controls, indicating that CB1 receptor antagonist pretreatments did not disrupt the acquisition of habituation. In two additional experiments, rats acquired habituation to loud noise drug free, then lower doses of AM251 (0.5 and 1.0 mg.kg) were administered before a final exposure (expression of habituation) to the homotypic stressor and/or a novel heterotypic stressor. CB1 receptor antagonism disrupted the expression of CORT response habituation and some of the c-fos mRNA reduction associated with it and facilitated novel stressor sensitization in doses that did not potentiate acute responses to these stressors. Collectively, these data suggest a progressive intensification of neural eCB signaling at CB1 receptors with repeated stress exposures.

Impact of Gruesome Photographic Evidence on Legal Decisions: A Meta-Analysis.

Gruesome crime scene and autopsy photographs are admissible evidence under the Federal Rules of Evidence (FRE) if their probative value substantially outweighs their prejudicial impact. Despite important methodological differences and mixed results from past studies, recommendations from the psychological literature have been made about the prejudicial impact of gruesome photographs perhaps prematurely. This meta-analysis investigates whether there is sufficient empirical evidence that presenting gruesome photographs in a trial affects legal decisions. The analysis of 23 studies and 4868 participants shows a small but statistically significant effect of gruesome photographs increasing guilty/liable verdicts or punishments, Hedge's g = 0.143, 95% CI: [0.055, 0.232]. However, this effect is significantly, Q(1) = 8.086, p = .004, and substantially moderated by an important methodological distinction: the effect is much larger when studies compare gruesome photographs with no photographs (g = 0.450) than when they are compared with neutral photographs (g = 0.077). These results suggest that gruesome photographs do increase affirmative verdicts, both through a small effect of gruesome content as well as a larger additive of having visual material. These findings help shed light on the mixed empirical results and suggest that important additional research is needed.

Accessory and main olfactory systems influences on predator odor-induced behavioral and endocrine stress responses in rats.

Exposures to predator odors are very effective methods to evoke a variety of stress responses in rodents. We have previously found that ferret odor exposure leads to changes in endocrine hormones (corticosterone and ACTH) and behavior. To distinguish the contributions of the main and accessory olfactory systems in these responses, studies were designed to interfere with these two systems either independently, or simultaneously. Male Sprague-Dawley rats were treated with 10% zinc sulfate (ZnSO(4)), which renders rodents anosmic (unable to smell) while leaving the accessory olfactory areas intact, or saline, in Experiment 1. In Experiment 2, the vomeronasal organs of rats were surgically removed (VNX) to block accessory olfactory processing, while leaving the main olfactory system intact. And in the third experiment both the main and accessory olfactory areas were disrupted by combining the two procedures in the same rats. Neither ZnSO(4) treatment nor VNX alone reliably reduced the increased corticosterone response to ferret odor compared to strawberry odor, but in combination, they did. This suggests that processing through the main or the accessory olfactory system can elicit the endocrine stress response to ferret odor. VNX alone also did not affect the behavioral responses to the ferret odor. ZnSO(4) treatment, alone and in combination with VNX, led to changes in behavior in response to both ferret and strawberry odor, making the behavioral results less clearly interpretable. Overall these studies suggest that both the main and accessory olfactory systems mediate the neuroendocrine response to predator odor.

Disruption of neuroendocrine stress responses to acute ferret odor by medial, but not central amygdala lesions in rats.

Investigations of the neural pathways associated with responses to predators have implicated the medial amygdala (MeA) as an important region involved in defensive behaviors. To our knowledge, however, the involvement of the MeA in neuroendocrine responses to predator odor exposure has not been investigated. Therefore, the present study examined the effects of MeA disruption in rats exposed to ferret or control odor on hypothalamo-pituitary-adrenocortical (HPA) axis activation. Bilateral lesions of the MeA were made in Sprague-Dawley rats with the neurotoxin ibotenic acid (10 microg/microl; 0.3 microl / side). As a control for regional specificity, additional groups of rats were given lesions in the central amygdala (CeA). One week after recovery, the rats were exposed to ferret or strawberry control towels in small cages to examine HPA axis responses as determined by plasma corticosterone and adrenocorticotropin hormone (ACTH) levels. Rats with complete bilateral MeA but not CeA lesions displayed significantly less corticosterone and ACTH release compared to sham-operated control rats only in the ferret odor conditions. These results suggest that the MeA is an important structure involved in the HPA axis responses to predator odors, in support of previous studies investigating behavioral responses under similar conditions.