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Reward System (reward + system)
Kinds of Reward System Selected AbstractsFROM BOYER'S SCHOLARSHIP OF TEACHING TO THE AACSB'S INSTRUCTIONAL DEVELOPMENT: IMPLICATIONS FOR FACULTY REWARD SYSTEMSJOURNAL OF LEGAL STUDIES EDUCATION, Issue 2 2000Marcia J. Staff Finally, the scholarship of teaching, in which research is conducted on effective and appropriate teaching methods, must be emphasized for all scholars. Teaching that is not grounded in the most recent research is not appropriate for a college or university setting. [source] Cognitive enhancement as a pharmacotherapy target for stimulant addictionADDICTION, Issue 1 2010Mehmet Sofuoglu ABSTRACT Background No medications have been proven to be effective for cocaine and methamphetamine addiction. Attenuation of drug reward has been the main strategy for medications development, but this approach has not led to effective treatments. Thus, there is a need to identify novel treatment targets in addition to the brain reward system. Aim To propose a novel treatment strategy for stimulant addiction that will focus on medications enhancing cognitive function and attenuating drug reward. Methods Pre-clinical and clinical literature on potential use of cognitive enhancers for stimulant addiction pharmacotherapy was reviewed. Results and conclusions Cocaine and methamphetamine users show significant cognitive impairments, especially in attention, working memory and response inhibition functions. The cognitive impairments seem to be predictive of poor treatment retention and outcome. Medications targeting acetylcholine and norepinephrine are particularly well suited for enhancing cognitive function in stimulant users. Many cholinergic and noradrenergic medications are on the market and have a good safety profile and low abuse potential. These include galantamine, donepezil and rivastigmine (cholinesterase inhibitors), varenicline (partial nicotine agonist), guanfacine (alpha2 -adrenergic agonist) and atomoxetine (norepinephrine transporter inhibitor). Future clinical studies designed optimally to measure cognitive function as well as drug use behavior would be needed to test the efficacy of these cognitive enhancers for stimulant addiction. [source] Startle cue,reactivity differentiates between light and heavy smokersADDICTION, Issue 10 2009Anne K. Rehme ABSTRACT Aims It was assumed that the startle amplitude in smokers is reduced while viewing pictures of smoking, suggesting that smoking cues are appetitive. The goal of the present study was to investigate (i) whether smoking scenes induce appetitive cue effects in smokers, and (ii) whether smoking intensity is related to cue,reactivity. Design Smokers and non-smokers participated in a single session. Participants A total of 62 individuals participated: 36 smokers and 26 non-smokers. Measurements Participants took part in an acoustic affective startle experiment using standardized pleasant, neutral and unpleasant scenes from the International Affective Picture System (IAPS), as well as pictures of smoking. The effect of smoking cues was assessed by comparing neutral and smoking scenes (termed cue-related startle suppression, CSS). Findings While there was no overall difference between smokers and non-smokers regarding the CSS, light smokers showed significantly increased cue,reactivity towards smoking-related cues, as compared with heavy smokers and non-smokers. In addition, light smokers also displayed stronger appetitive responses towards positive stimuli. Conclusions These data support recent theories which discriminate between habit-based and incentive-based drug abuse. This distinction may have consequences for the assessment and treatment of drug-addicted subjects. Furthermore, incentive-based light smoking seems to have general effects on the reward system. [source] PRECLINICAL STUDY: FULL ARTICLE: Effects of fatty acid amide hydrolase inhibition on neuronal responses to nicotine, cocaine and morphine in the nucleus accumbens shell and ventral tegmental area: involvement of PPAR-, nuclear receptorsADDICTION BIOLOGY, Issue 3 2010Antonio Luchicchi ABSTRACT The endocannabinoid system regulates neurotransmission in brain regions relevant to neurobiological and behavioral actions of addicting drugs. We recently demonstrated that inhibition by URB597 of fatty acid amide hydrolase (FAAH), the main enzyme that degrades the endogenous cannabinoid N-acylethanolamine (NAE) anandamide and the endogenous non-cannabinoid NAEs oleoylethanolamide and palmitoylethanolamide, blocks nicotine-induced excitation of ventral tegmental area (VTA) dopamine (DA) neurons and DA release in the shell of the nucleus accumbens (ShNAc), as well as nicotine-induced drug self-administration, conditioned place preference and relapse in rats. Here, we studied whether effects of FAAH inhibition on nicotine-induced changes in activity of VTA DA neurons were specific for nicotine or extended to two drugs of abuse acting through different mechanisms, cocaine and morphine. We also evaluated whether FAAH inhibition affects nicotine-, cocaine- or morphine-induced actions in the ShNAc. Experiments involved single-unit electrophysiological recordings from DA neurons in the VTA and medium spiny neurons in the ShNAc in anesthetized rats. We found that URB597 blocked effects of nicotine and cocaine in the ShNAc through activation of both surface cannabinoid CB1-receptors and alpha-type peroxisome proliferator-activated nuclear receptor. URB597 did not alter the effects of either cocaine or morphine on VTA DA neurons. These results show that the blockade of nicotine-induced excitation of VTA DA neurons, which we previously described, is selective for nicotine and indicate novel mechanisms recruited to regulate the effects of addicting drugs within the ShNAc of the brain reward system. [source] PRECLINICAL STUDY: FULL ARTICLE: Ghrelin increases intake of rewarding food in rodentsADDICTION BIOLOGY, Issue 3 2010Emil Egecioglu ABSTRACT We investigated whether ghrelin action at the level of the ventral tegmental area (VTA), a key node in the mesolimbic reward system, is important for the rewarding and motivational aspects of the consumption of rewarding/palatable food. Mice with a disrupted gene encoding the ghrelin receptor (GHS-R1A) and rats treated peripherally with a GHS-R1A antagonist both show suppressed intake of rewarding food in a free choice (chow/rewarding food) paradigm. Moreover, accumbal dopamine release induced by rewarding food was absent in GHS-R1A knockout mice. Acute bilateral intra-VTA administration of ghrelin increased 1-hour consumption of rewarding food but not standard chow. In comparison with sham rats, VTA-lesioned rats had normal intracerebroventricular ghrelin-induced chow intake, although both intake of and time spent exploring rewarding food was decreased. Finally, the ability of rewarding food to condition a place preference was suppressed by the GHS-R1A antagonist in rats. Our data support the hypothesis that central ghrelin signaling at the level of the VTA is important for the incentive value of rewarding food. [source] REVIEW: Identifying the neural circuitry of alcohol craving and relapse vulnerabilityADDICTION BIOLOGY, Issue 1 2009Andreas Heinz ABSTRACT With no further intervention, relapse rates in detoxified alcoholics are high and usually exceed 80% of all detoxified patients. It has been suggested that stress and exposure to priming doses of alcohol and to alcohol-associated stimuli (cues) contribute to the relapse risk after detoxification. This article focuses on neuronal correlates of cue responses in detoxified alcoholics. Current brain imaging studies indicate that dysfunction of dopaminergic, glutamatergic and opioidergic neurotransmission in the brain reward system (ventral striatum including the nucleus accumbens) can be associated with alcohol craving and functional brain activation in neuronal systems that process attentional relevant stimuli, reward expectancy and experience. Increased functional brain activation elicited by such alcohol-associated cues predicted an increased relapse risk, whereas high brain activity elicited by affectively positive stimuli may represent a protective factor and was correlated with a decreased prospective relapse risk. These findings are discussed with respect to psychotherapeutic and pharmacological treatment options. [source] Reduced operant ethanol self-administration and in vivo mesolimbic dopamine responses to ethanol inPKC,-deficient miceEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2000M. Foster Olive Abstract There is increasing evidence that individual protein kinase C (PKC) isozymes mediate specific effects of ethanol on the nervous system. In addition, multiple lines of evidence suggest that the mesoaccumbens dopamine reward system is critically involved in the rewarding and reinforcing effects of ethanol. Yet little is known about the role of individual PKC isozymes in ethanol reinforcement processes or in regulation of mesolimbic systems. In this study, we report that mice lacking the epsilon isoform of PKC (PKC,) show reduced operant ethanol self-administration and an absence of ethanol-induced increase in extracellular dopamine levels in the nucleus accumbens. PKC, null mice exhibited a 53% decrease in alcohol-reinforced operant responses under basal conditions, as well as following ethanol deprivation. Behavioural analysis revealed that while both genotypes had the same number of drinking bouts following deprivation, PKC, null mice demonstrated a 61% reduction in number of ethanol reinforcers per bout and a 57% reduction in ethanol-reinforced response rate. In vivo microdialysis experiments showed that, in contrast to wild-type mice, PKC, null mice exhibited no change in extracellular levels of dopamine in the nucleus accumbens following acute administration of ethanol (1 and 2 g/kg i.p.), while mesolimbic dopamine responses to cocaine (20 mg/kg i.p.) or high potassium (100 m m) in these mice were comparable with that of wild-types. These data provide further evidence that increases in extracellular mesolimbic dopamine levels contribute to the reinforcing effects of ethanol, and indicate that pharmacological agents inhibiting PKC, may be useful in the treatment of alcohol dependence. [source] Altered representation of expected value in the orbitofrontal cortex in maniaHUMAN BRAIN MAPPING, Issue 7 2010Felix Bermpohl Abstract Objective: Increased responsiveness to appetitive and reduced responsiveness to aversive anticipatory cues may be associated with dysfunction of the brain reward system in mania. Here we studied neural correlates of gain and loss expectation in mania using functional magnetic resonance imaging (fMRI). Method: Fifteen manic patients and 26 matched healthy control individuals performed a monetary incentive delay task, during which subjects anticipated to win or lose a varying amount of money. Varying both magnitude and valence (win, loss) of anticipatory cues allowed us to isolate the effects of magnitude, valence and expected value (magnitude-by-valence interaction). Results: Response times and total gain amount did not differ significantly between groups. FMRI data indicated that the ventral striatum responded according to cued incentive magnitude in both groups, and this effect did not significantly differ between groups. However, a significant group difference was observed for expected value representation in the left lateral orbitofrontal cortex (OFC; BA 11 and 47). In this region, patients showed increasing BOLD responses during expectation of increasing gain and decreasing responses during expectation of increasing loss, while healthy subjects tended to show the inverse effect. In seven patients retested after remission OFC responses adapted to the response pattern of healthy controls. Conclusions: The observed alterations are consistent with a state-related affective processing bias during the expectation of gains and losses which may contribute to clinical features of mania, such as the enhanced motivation for seeking rewards and the underestimation of risks and potential punishments. Hum Brain Mapp, 2010. © 2009 Wiley-Liss, Inc. [source] An investigation into food preferences and the neural basis of food-related incentive motivation in Prader,Willi syndromeJOURNAL OF INTELLECTUAL DISABILITY RESEARCH, Issue 9 2006E. C. Hinton Abstract Background Research into the excessive eating behaviour associated with Prader,Willi syndrome (PWS) to date has focused on homeostatic and behavioural investigations. The aim of this study was to examine the role of the reward system in such eating behaviour, in terms of both the pattern of food preferences and the neural substrates of incentive in the amygdala and orbitofrontal cortex (OFC). Method Participants with PWS (n = 18) were given a food preference interview to examine food preferences and to inform the food-related incentive task to be conducted during the neuroimaging. Thirteen individuals with PWS took part in the positron emission tomography (PET) study, the design of which was based on a previous study of non-obese, non-PWS controls. For the task, participants were asked to consider photographs of food and to choose the food they would most like to eat in two conditions, one of high and one of low incentive foods, tailored to each participant's preferences. For comparison of the food preference data, 12 non-PWS individuals were given one part of the interview. Results Individuals with PWS expressed relative liking of different foods and showed preferences that were consistent over time, particularly for sweet foods. The participants with PWS did give the foods in the high incentive condition a significantly higher incentive value than the foods in the low incentive condition. However, activation of the amygdala and medial OFC was not associated with the prospect of highly valued foods as predicted in those with PWS. Conclusions It would appear that incentive motivation alone plays a less powerful role in individuals with PWS than in those without the syndrome. This is likely to be due to the overriding intrinsic drive to eat because of a lack of satiety in those with PWS, and the impact of this on activity in the incentive processing regions of the brain. Activity in such reward areas may not then function to guide behaviour selectively towards the consumption of high preference foods. [source] Individual Differences in Alcohol Drinking Frequency Are Associated With Electrophysiological Responses to Unexpected NonrewardsALCOHOLISM, Issue 4 2010Ingmar H. A. Franken Background:, It has been suggested that alcohol use is related to sensitivity of the reward system. Although there are several studies using self-reported measures supportive of this notion, objective biological data in humans on this issue are lacking. Aims:, This study is designed to test whether alcohol drinking frequency is associated with electrophysiological indices of reward processing. Materials and Methods:, In a passive gambling task, stimuli predicted the presence (reward) and absence (nonreward) of rewards resulting in P2 and medial frontal negativity (MFN) indices of reward processing. Forty-seven undergraduate students were asked about their habitual drinking frequency and the P2 and MFN to stimuli predicting reward were measured. Results:, Most importantly, the MFN to unpredicted nonrewards at the frontal midline (Fz) location correlated significantly with drinking frequency, with frequent drinkers showing larger MFN amplitudes. The results did not show a significant association between frequency and alcohol drinking and P2. Discussion:, Although several studies showing increased reward-sensitivity in addictive behaviors, the present results indicate that, in frequent alcohol drinkers, electrophysiological responsiveness is particularly activated by unpredicted nonrewards. In general, this may point to the involvement of the reward system in alcohol drinking frequency. Conclusion:, More specifically, the results demonstrate an increased vulnerability of high frequency drinkers to signals of (frustrative) nonrewards. [source] The Glycine Reuptake Inhibitor Org 25935 Interacts With Basal and Ethanol-Induced Dopamine Release in Rat Nucleus AccumbensALCOHOLISM, Issue 7 2009Helga Höifödt Lidö Background:, The mesolimbic dopamine (DA) projection from the ventral tegmental area to nucleus accumbens (nAc), a central part of the reward system, is activated by ethanol (EtOH) and other drugs of abuse. We have previously demonstrated that the glycine receptor in the nAc and its amino acid agonists may be implicated in the DA activation and reinforcing properties of EtOH. We have also reported that the glycine transporter 1 inhibitor, Org 25935, produces a robust and dose-dependent decrease in EtOH consumption in Wistar rats. The present study explores the interaction between EtOH and Org 25935 with respect to DA levels in the rat nAc. Methods:, The effects of Org 25935 (6 mg/kg, i.p.) and/or EtOH (2.5 g/kg, i.p.) on accumbal DA levels were examined by means of in vivo microdialysis (coupled to HPLC-ED) in freely moving male Wistar rats. The effect of Org 25935 on accumbal glycine output was also investigated. Results:, Systemic Org 25935 increased DA output in a subpopulation of rats (52% in Experiment 1 and 38% in Experiment 2). In Experiment 2, EtOH produced a significant increase in DA levels in vehicles (35%) and in Org 25935 nonresponders (19%), whereas EtOH did not further increase the DA level in rats responding to Org 25935 (2%). The same dose of Org 25935 increased glycine levels by 87% in nAc. Conclusions:, This study demonstrates that Org 25935, probably via increased glycine levels, (i) counteracts EtOH-induced increases of accumbal DA levels and (ii) increases basal DA levels in a subpopulation of rats. The results are in line with previous findings and it is suggested that the effects observed involve interference with accumbal GlyRs and are related to the alcohol consumption modulating effect of Org 25935. [source] Ethanol-Sensitive Brain Regions in Rat and Mouse: A Cartographic Review, Using Immediate Early Gene ExpressionALCOHOLISM, Issue 6 2009Catherine Vilpoux Background:, Ethanol addiction has been conceptualized as a progression from occasional, impulsive use to compulsive behavior. Ethanol-dependence is a chronic pathology with repeated cycles of withdrawal, craving, and relapse. Specific molecular and cellular mechanisms underlie these transition stages. Methods:, This review aimed at elucidating whether there are also adaptations in the pattern of brain regions responding to ethanol. This paper reviews the evidence in rodents for activation of specific brain regions, assessed by induction of IEG expression, following acute and chronic ethanol exposure. Results:, The review sheds light on the specific patterns of response in regions of the brain to different types of ethanol exposure and shows that activation of specific brain regions may occur in particular phases of the development of ethanol addiction. Some brain regions respond consistently following acute or chronic treatments or withdrawal: the prefrontal cortex; nucleus accumbens; lateral septum; hippocampus; perioculomotor urocortin-containing cells population (pIIIu), also known as Edinger-Westphal nucleus; central nucleus of the amygdale; and the paraventricular nucleus of hypothalamus. The two last brain areas are particularly activated by relapse-inducing stressors. It is of interest that the amygdala, hippocampus, and prefrontal cortex, which belong to the reward system, are activated by cue-induced relapse to ethanol self-administration in rodents and humans, while activation of these regions is reversed with anticraving compounds. Following chronic exposure, IEG induction desensitizes while withdrawal reactivates these regions. Discussion:, Some responding regions are implicated in reward related processes (VTA, extended amygdala, hypothalamus, hippocampus, prelimbic cortex, ventral part of lateral septum) and some others in aversive-related processes (area postrema, nucleus of solitary tract). Conclusion:, A better understanding of the neural circuits affected by ethanol and their adaptations during the development of ethanol addiction will provide new opportunities for developing appropriate therapies. [source] An exploration of mental health nursing students' experiences and attitudes towards using cigarettes to change client's behaviourJOURNAL OF PSYCHIATRIC & MENTAL HEALTH NURSING, Issue 8 2010M. J. NASH msc pclt bsc (hons) rnt rmn fhea Accessible summary ,,This study explores the experiences of mental health nursing students in using cigarettes as a means of token economy. ,,The majority of the sample experienced the use of this particular intervention in various settings but also reported that other items apart from cigarettes were also used as part of a reward system. ,,Respondents generally did not like this practice, feeling that it did not work well, led to client staff conflict, was implemented in an ad hoc way and rarely recorded in a care plan. ,,An open debate on tobacco control and the use of cigarettes in behavioural change programmes is urgently required. Abstract Using cigarettes to change client behaviour is a common, yet little studied, practice in mental health care. A questionnaire survey was used to explore mental health nursing student's experiences and attitudes to this practice. The sample was four cohorts of mental health nursing students (n= 151). Of them, 84% had experienced the practice of using cigarettes to change client behaviour in acute wards (73%), rehabilitation wards (28%) and elderly care (14%). Cigarettes were used to change client behaviour in areas such as attending to personal hygiene (57%) or engaging in the ward routine (39%). However, items such as leave (60%) or drinks (tea and coffee) (38%) were also reportedly used. Of the respondents, 54% inferred that the practice did not work well with 46% stating it was not written up in care plans; 52% felt it was an ad hoc practice, 60% inferred that at times it was used as a punishment while 55% intimated that they felt bad withholding cigarettes. There are ethical and moral dilemmas around using lifestyle risk factors as rewards or using client's nicotine addiction as a means of controlling behaviour. The question of whether this intervention should ever be used, given its associated health risk, requires more critical debate in clinical practice. [source] Frontal White Matter and Cingulum Diffusion Tensor Imaging Deficits in AlcoholismALCOHOLISM, Issue 6 2008Gordon J. Harris Background:, Alcoholism-related deficits in cognition and emotion point toward frontal and limbic dysfunction, particularly in the right hemisphere. Prefrontal and anterior cingulate cortices are involved in cognitive and emotional functions and play critical roles in the oversight of the limbic reward system. In the present study, we examined the integrity of white matter tracts that are critical to frontal and limbic connectivity. Methods:, Diffusion tensor magnetic resonance imaging (DT-MRI) was used to assess functional anisotropy (FA), a measure of white matter integrity, in 15 abstinent long-term chronic alcoholic and 15 demographically equivalent control men. Voxel-based and region-based analyses of group FA differences were applied to these scans. Results:, Alcoholic subjects had diminished frontal lobe FA in the right superior longitudinal fascicles II and III, orbitofrontal cortex white matter, and cingulum bundle, but not in corresponding left hemisphere regions. These right frontal and cingulum white matter regional FA measures provided 97% correct group discrimination. Working Memory scores positively correlated with superior longitudinal fascicle III FA measures in control subjects only. Conclusions:, The findings demonstrate white matter microstructure deficits in abstinent alcoholic men in several right hemisphere tracts connecting prefrontal and limbic systems. These white matter deficits may contribute to underlying dysfunction in memory, emotion, and reward response in alcoholism. [source] When Changing from Merit Pay to Variable/Bonus Pay: What Do Employees Want?PERFORMANCE IMPROVEMENT QUARTERLY, Issue 4 2004Jeremy B. Fox ABSTRACT This study examines potential responses to a change in an employee reward system from permanent merit pay increases to one-time bonus payments. Removing long term risks associated with escalating pay is an increasingly common compensation strategy. Often overlooked, however, are employee perceptions of reward fairness under such conditions of change. Receiving lump sum payments in lieu of permanent merit pay increase may de-motivate employees. There has been little or no research conducted on this topic. In this study, using samples of practicing HR managers and university students, an equity questionnaire gathered data on the perceived equivalence between a permanent merit pay increase and what might be demanded by employees as a single payment in its replacement. An analysis of the data collected indicate an approximate 1:2 ratio is needed, such that a proposed lump-sum payment of $2400 would be perceived as a fair replacement for a permanent merit pay allocation of $1200 per year. Our research indicates that this 1:2 ratio holds for both high and low job satisfaction levels. [source] How Palatable Food Disrupts Appetite RegulationBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2005Charlotte Erlanson-Albertsson Hunger signals may be generated in peripheral organs (e.g. ghrelin) but most of them are expressed in the hypothalamus (neuropeptide Y, orexins, agouti-related peptide, melanin concentrating hormone, endogenous opiates and dopamine) and are expressed during situations of energy deficiency. Some satiety signals, such as cholecystokinin, glucagon-like peptide 1, peptide YY and enterostatin are released from the digestive tract in response to food intake. Others, such as leptin and insulin, are mobilized in response to perturbations in the nutritional state. Still others are generated in neurones of the hypothalamus (,-melanocyte-stimulating hormone and serotonin). Satiety signals act by inhibiting the expression of hunger signals and/or by blunting their effect. Palatable food, i.e. food rich in fat and sugar, up-regulates the expression of hunger signals and satiety signals, at the same time blunting the response to satiety signals and activating the reward system. Hence, palatable food offsets normal appetite regulation, which may explain the increasing problem of obesity worldwide. [source] Clinical Psychology in Academic DepartmentsCLINICAL PSYCHOLOGY: SCIENCE AND PRACTICE, Issue 3 2006Karen S. Calhoun This article discusses issues and future directions for clinical psychology in academic departments of psychology. Psychology continues to be the most popular undergraduate major and departments must better prepare them for graduate study. Budget constraints continue to impact departments, resulting in challenges such as decreasing numbers of faculty, increasing dependence on external grant funds, and accompanying distortion of the reward system for faculty contributions. Increasing specialization in clinical psychology will require difficult choices. Increasing emphasis on multidisciplinary study presents both opportunities and challenges for traditional departments of psychology. The emergence of neuroscience is having a great impact and the integration of psychology and neuroscience will be a significant issue facing clinical programs. Despite challenges, academic clinical psychology can be expected to remain resilient in the face of change. [source] PRECLINICAL STUDY: Ghrelin administration into tegmental areas stimulates locomotor activity and increases extracellular concentration of dopamine in the nucleus accumbensADDICTION BIOLOGY, Issue 1 2007Elisabet Jerlhag ABSTRACT Ghrelin stimulates appetite, increases food intake and causes adiposity by mechanisms that include direct actions on the brain. Previously, we showed that intracerebroventricular administration of ghrelin has stimulatory and dopamine-enhancing properties. These effects of ghrelin are mediated via central nicotine receptors, suggesting that ghrelin can activate the acetylcholine,dopamine reward link. This reward link consists of cholinergic input from the laterodorsal tegmental area (LDTg) to the mesolimbic dopamine system that originates in the ventral tegmental area (VTA) and projects to the nucleus accumbens. Given that growth hormone secretagogue receptors (GHSR-1A) are expressed in the VTA and LDTg, brain areas involved in reward, the present series of experiments were undertaken to examine the hypothesis that these regions may mediate the stimulatory and dopamine-enhancing effects of ghrelin, by means of locomotor activity and in vivo microdialysis in freely moving mice. We found that local administration of ghrelin into the VTA (1 µg in 1 µl) induced an increase in locomotor activity and in the extracellular concentration of accumbal dopamine. In addition, local administration of ghrelin into the LDTg (1 µg in 1 µl) caused a locomotor stimulation and an increase in the extracellular levels of accumbal dopamine. Taken together, this indicates that ghrelin might, via activation of GHSR-1A in the VTA and LDTg, stimulate the acetylcholine,dopamine reward link, implicating that ghrelin is a part of the neurochemical overlap between the reward systems and those that regulate energy balance. [source] Pseudoparadoxical impulsivity in restrictive anorexia nervosa: A consequence of the logic of scarcityINTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 4 2002Daniel M. T. Fessler Abstract Objective To explain an apparently paradoxical pattern wherein sufferers of restrictive anorexia nervosa exhibit both rigorous self-restraint and episodic impulsivity. Method The experimental, historical, and clinical literatures were examined for evidence of psychological and behavioral changes accompanying severe dietary constriction; such changes were noted and compared with those reported to occur in anorexics. Results Increased impulsivity in association with dietary constriction is described in diverse literatures. A number of lines of evidence suggest that the serotonergic system mediates this change. Discussion Many forms of impulsivity can be understood as having once constituted fitness-enhancing responses to resource scarcity. It is suggested that an evolved psychological mechanism calibrates the individual's sensitivity to risk in light of future prospects. Self-injurious behaviors are explicable as misfirings of such a mechanism. Similarly, excessive exercising by anorexics may reflect the misdirection of reward systems that normally encourage adaptive increases in ranging behavior under conditions of scarcity. © 2002 by Wiley Periodicals, Inc. Int J Eat Disord 31: 376,388, 2002. [source] Interdependence as a Moderator of the Relationship Between Competitiveness and Objective Sales PerformanceINTERNATIONAL JOURNAL OF SELECTION AND ASSESSMENT, Issue 4 2005Chet Robie In this study, we investigated the moderating role of interdependence (a personality trait that measures the extent to which individuals desire working in a group-based, cooperative setting) on the relationship between competitiveness and one-year objective sales performance. On the basis of data from 133 sales representatives, results indicated that: (a) competitiveness was related to objective sales performance; and (b) interdependence moderated the relationship between competitiveness and objective sales performance such that competitiveness predicted objective sales performance more strongly for those who scored low in interdependence versus those who scored high in interdependence. Implications for sales selection and reward systems and directions for future research are considered. [source] To prosper, organizational psychology should, bridge application and scholarship,JOURNAL OF ORGANIZATIONAL BEHAVIOR, Issue 4 2008Wayne F. Cascio Academics and practitioners differ on so many dimensions that researchers have described them as living in different "thought worlds." That gap persists, and there are important explanations for it, but a confluence of economic and organizational forces is driving academics and practitioners toward each other. To date, much of the effort by academics to reach out to practitioners has focused on the diffusion of scientific knowledge, not its creation. This paper explores several promising strategies for improving both the bidirectional diffusion of knowledge as well as its creation. It argues that for genuine change to occur, it is necessary to modify academic reward systems and to promote much closer collaboration between academics and practitioners. Copyright © 2008 John Wiley & Sons, Ltd. [source] Chronic nicotine treatment changes the axonal distribution of 68 kDa neurofilaments in the rat ventral tegmental areaEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2002Andrea Sbarbati Abstract Region-specific decreases of neurofilament proteins (NF) were described in the ventral tegmental area (VTA) of rats treated chronically with morphine, cocaine or alcohol. In a previous study, we demonstrated that NF levels were also changed in the VTA after chronic treatment with nicotine. The aim of this study was to clarify the submicroscopic basis of decreased immunoreactivity for NF-68, NF-160 and NF-200, as determined by using NR4, BF10 and RT97 antibodies, respectively. Microdensitometric analysis of brain sections showed that immunoreactivity for all NF was reduced in the VTA of animals exposed chronically to nicotine (0.4 mg/kg per day, 6 days of treatment), when compared to rats exposed to saline. Reduction in immunoreactivity was significant for NF-68 (P < 0.05), NF-160 (P < 0.01) and NF-200 (P < 0.05), showing a relative reduction of 34%, 42% and 38%, respectively, when compared to saline-treated rats. No difference was observed for any of the NF under study when immunoreactivity measurements in the substantia nigra were compared. Ultrastructural analysis was applied to evaluate changes in NF-68, NF-160 and NF-200 immunoreactivity in regions of the VTA that contain dopaminergic neurons following chronic nicotine treatment. At the electron microscopic level, no degenerative changes were found in neurons or glial cells of the VTA. With ultrastructural immunohistochemistry, evaluation of the homogeneity parameter of NF distribution showed a loss of homogeneity for NF-68 linked to the nicotine treatment. In areas in which NF organization appeared well preserved, analysis of the numerical density of NF revealed no significant difference for NF-68 (897/µm2 vs. 990/µm2), NF-160 (970/µm2 vs. 820/µm2) and NF-200 (1107/µm2 vs. 905/µm2) in nicotine-treated rats when compared to saline-treated rats. These results confirm that nicotine shares the same properties with cocaine and morphine in reducing NF in the VTA, a key brain structure of the rewards system, and that chronic nicotine treatment changes the axonal distribution of 68 kDa neurofilaments in the rat VTA. [source] Motivators and Inhibitors for University Faculty in Distance and e-learningBRITISH JOURNAL OF EDUCATIONAL TECHNOLOGY, Issue 1 2009Ruth Gannon Cook This article reports on four United States studies of how rewards systems, extrinsic and intrinsic, could play an important role in providing incentives for university faculty to teach (or remain teaching) electronic and distance education courses. The first three studies conducted prior to 2003 reported faculty were inherently motivated to teach e-learning and distance education. The fourth study in 2003 reported key findings that differed from the earlier studies. Using a principal components analysis, the researchers found nine indicators of motivation to participate or not participate in electronic or distance education. The implications from the fourth study indicated that, while faculty members were inherently committed to helping students, faculty members wanted their basic physiological needs met by university administration through extrinsic motivators, such as salary increases and course releases. [source] | ||||||||||||||||||||||