Determination of interaction effects in expectations for post-event information on memory for items in a service encounter

Our minds are not a blank canvas onto which experiences leave their independent and indelible impression. Consumers, therefore, would rarely enter a service encounter without prior knowledge to guide their expectations. The importance of prior knowledge – in the form of schemas – while acknowledged in the study of post-event misinformation effects on memory has received limited attention. Outside of studies investigating misinformation effects, the literature indicates that inconsistency between our expectations and what we experience, improves recall accuracy. Whether this effect translates into reduced susceptibility to misinformation effects and that schema consistency increases susceptibility, is unclear. The main contribution of this thesis is the demonstration that consistency between schema and the experience, and its interaction with encoding goals, changes a person’s susceptibility to misinformation and their subsequent store quality perceptions. The effects of encoding goals – whether someone is trying to form an impression or remember the details of their experience – while used in previous misinformation studies, has not been previously investigated. To investigate the effects of schema consistency and encoding goals on misinformation acceptance, and the subsequent impact of misinformation acceptance on store quality perceptions, a three-way between participant design was undertaken using a café service encounter as the context. The three factors – independent variables – and their levels included in the study were schema consistency (consistent/ inconsistent), encoding goal (impression/ recall) and post-event information (misinformation/ neutral). Results from the study showed that misinformation effects are most likely when people are paying less attention to the service environment. The explanation provided in the study is that when there is a match between what people expect and what they experience they pay less attention to the details of the experience, which results in less diagnostic information encoded into memory. If, however, they were paying attention due to an inconsistency, the information would be attended and result in reduced misinformation acceptance. Where a person was instructed to try and remember the details of their experience rather than form an impression, they paid greater attention to detail than those who were forming an impression. When their expectations were not met in an experience, subsequent exposure to misinformation causes these people to accurately recall their original experience and escape the effect of misinformation. Significant results were also observed for changes to store quality perceptions, revealing that consumers who accept the misinformation have store quality perceptions that reflect its inclusion. Also observed was an interaction with the initial expectations that meant merchandise quality perceptions improved when a person’s memory for the experience was consistent with their original expectations, and lower when inconsistent

Role of the endocannabinoid system in regulating glucocorticoid effects on memory for emotional experiences

Item does not contain fulltextGlucocorticoids, stress hormones released from the adrenal cortex, have potent modulatory effects on emotional memory. Whereas early studies focused mostly on the detrimental effects of chronic stress and glucocorticoid exposure on cognitive performance and the classic genomic pathways that mediate these effects, recent findings indicate that glucocorticoids exert complex and often rapid influences on distinct memory phases. Specifically, glucocorticoids have been shown to enhance memory consolidation of emotionally arousing experiences, but to impair memory retrieval and working memory during emotionally arousing test situations. Furthermore, growing evidence indicates that these different glucocorticoid effects depend on a nongenomically mediated interaction with emotional arousal-induced noradrenergic activation within the basolateral complex of the amygdala. In this paper, we present a model suggesting that the endocannabinoid system, a lipid-based retrograde signaling system, might play an important role in mediating such rapid glucocorticoid influences on the noradrenergic system in modulating memory of emotionally arousing experiences

Effect of ingested sulfite on hippocampus antioxidant enzyme activities in sulfite oxidase competent and deficient rats.

Animal tissues are exposed to sulfite used as a preservative in food and drugs, and generated from the catabolism of sulfur-containing amino acids. Sulfite, which is a very reactive and potentially toxic molecule, is detoxified by the enzyme sulfite oxidase (SOX). Laboratory animals can be made deficient in SOX by the administration of a high-tungsten/low molybdenum regimen. It has been suggested that SOX deficient rats might be used as a model for the prediction of sulfite toxicity in humans. The aim of this study was to investigate the effects of ingested sulfite on hippocampus superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in SOX competent and deficient rats. Hippocampus SOD, CAT and GPx activities were found to be significantly increased by sulfite treatment in SOX competent groups. On the other hand, exposure to sulfite had no effect on antioxidant status in hippocampus of SOX deficient rats. In conclusion, these results suggest that hippocampus antioxidant capacity where defense mechanism against the oxidative challenge is up regulated by sulfite in SOX competent rats. This up regulation mechanism in antioxidant enzymes against to sulfite related oxidative stress is not observed in SOX deficient rats and remains to be explained

in sulfite oxidase competent and deficient rats

Animal tissues are exposed to sulfite used as a preservative in food and drugs, and generated from the catabolism of sulfur-containing amino acids. Sulfite, which is a very reactive and potentially toxic molecule, is detoxified by the enzyme sulfite oxidase (SOX). Laboratory animals can be made deficient in SOX by the administration of a high-tungsten/low molybdenum regimen. It has been suggested that SOX deficient rats might be used as a model for the prediction of sulfite toxicity in humans. The aim of this study was to investigate the effects of ingested sulfite on hippocampus superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in SOX competent and deficient rats. Hippocampus SOD, CAT and GPx activities were found to be significantly increased by sulfite treatment in SOX competent groups. On the other hand, exposure to sulfite had no effect on antioxidant status in hippocampus of SOX deficient rats. In conclusion, these results suggest that hippocampus antioxidant capacity where defense mechanism against the oxidative challenge is up regulated by sulfite in SOX competent rats. This up regulation mechanism in antioxidant enzymes against to sulfite related oxidative stress is not observed in SOX deficient rats and remains to be explained.C1 Pamukkale Univ, Fac Med, Dept Physiol, TR-20020 Denizli, Turkey.Akdeniz Univ, Fac Med, Dept Physiol, Antalya, Turkey

parameters in rats

Aluminum (Al) is a nonessential element and humans are constantly exposed to Al as a result of an increase in industrialization and improving technology practices. Al toxicity can induce several clinical disorders such as neurotoxicity, gastrointestinal toxicity, hepatotoxicity, bone diseases, and anemia. This study aimed at evaluating the possible effects of short term and low dose Al exposure on hemorheological and hematological parameters in rats. Fourteen young, male Wistar albino rats were divided into two groups: 1 mg/200 g body weight of aluminum sulfate (Al-2(SO4)(3) was injected intraperitoneally to the first group for two weeks, three times a week. The animals of the control group received only physiological saline solution during this period. At the end of the experimental period, anticoagulated blood samples were collected and hematological parameters were determined using an electronic hematology analyzer. Red blood cell (RBC) deformability and aggregation were measured using an ektacytometer (LORCA) and plasma and whole blood viscosities were determined with a Wells-Brookfield cone-plate rotational viscometer. Significant decreases in mean corpuscular volume (MCV), red blood cell (RBC) deformability at low shear stress levels, the aggregation half time (t1/2) and the amplitude (AMP) of aggregation and significant increments in whole blood viscosity (WBV) at native and 40% hematocrit (Hct) of Al-treated rats have been observed. In conclusion, low dose Al-2(SO4)(3) exposure for a short-time may be responsible for alterations in either rheological properties of blood or hemorheological properties through a remarkable effect on RBC membrane mechanical properties .These alterations may also play an important role in the development of anemia in the Al-treated animals

The effects of low dose aluminum on hemorheological and hematological parameters in rats.

Aluminum (Al) is a nonessential element and humans are constantly exposed to Al as a result of an increase in industrialization and improving technology practices. Al toxicity can induce several clinical disorders such as neurotoxicity, gastrointestinal toxicity, hepatotoxicity, bone diseases, and anemia. This study aimed at evaluating the possible effects of short term and low dose Al exposure on hemorheological and hematological parameters in rats. Fourteen young, male Wistar albino rats were divided into two groups: 1 mg/200 g body weight of aluminum sulfate (Al(2)(SO(4))(3) was injected intraperitoneally to the first group for two weeks, three times a week. The animals of the control group received only physiological saline solution during this period. At the end of the experimental period, anticoagulated blood samples were collected and hematological parameters were determined using an electronic hematology analyzer. Red blood cell (RBC) deformability and aggregation were measured using an ektacytometer (LORCA) and plasma and whole blood viscosities were determined with a Wells-Brookfield cone-plate rotational viscometer. Significant decreases in mean corpuscular volume (MCV), red blood cell (RBC) deformability at low shear stress levels, the aggregation half time (t1/2) and the amplitude (AMP) of aggregation and significant increments in whole blood viscosity (WBV) at native and 40% hematocrit (Hct) of Al-treated rats have been observed. In conclusion, low dose Al(2)(SO(4))(3) exposure for a short-time may be responsible for alterations in either rheological properties of blood or hemorheological properties through a remarkable effect on RBC membrane mechanical properties . These alterations may also play an important role in the development of anemia in the Al-treated animals

Stress and Memory: A Selective Review on Recent Developments in the Understanding of Stress Hormone Effects on Memory and Their Clinical Relevance

Item does not contain fulltextStress causes a neuroendocrine response cascade, leading to the release of catecholamines and glucocorticoids (GCs). GCs influence learning and memory by acting on mineralocorticoid (MR) and glucocorticoid (GR) receptors. Typically, GCs enhance the consolidation of memory processing at the same time as impairing the retrieval of memory of emotionally arousing experiences. The present selective review addresses four recent developments in this area. First, the role of the endocannabinoid system in mediating the rapid, nongenomic effects of GCs on memory is illustrated in rodents. Subsequently, studies on the impact of the selective stimulation of MRs on different memory processes in humans are summarised. Next, a series of human experiments on the impact of stress or GC treatment on fear extinction and fear reconsolidation is presented. Finally, the clinical relevance of the effects of exogenous GC administration is highlighted by the description of patients with anxiety disorders who demonstrate an enhancement of extinction-based therapies by GC treatment. The review highlights the substantial progress made in our mechanistic understanding of the memory-modulating properties of GCs, as well as their clinical potential