Resistance to extinction after schedules of partial delay or partial reinforcement in rats with hippocampal lesions

Summary Two experimental procedures were employed to establish the reason why hippocampal lesions apparently block the development of tolerance for aversive events in partial reinforcement experiments, but do not do so in partial punishment experiments. Rats were trained to run in a straight alley following hippocampal lesions (HC), cortical control lesions (CC) or sham operations (SO), and resistance to extinction was assessed following differing acquisition conditions. In Experiment 1 a 4–8 min inter-trial interval (ITI) was used. Either every acquisition trial was rewarded immediately (Continuous Reinforcement, CR), or only a randomly selected half of the trials were immediately rewarded, the reward being delayed for thirty seconds on the other trials (Partial Delay, PD). This delay procedure produced increased resistance to extinction in rats in all lesion groups. In Experiment 2 the ITI was reduced to a few seconds, and rats were trained either on a CR schedule, or on a schedule in which only half the trials were rewarded (Partial Reinforcement, PR). This form of partial reinforcement procedure also produced increased resistance to extinction in rats in all lesion groups. It thus appears that hippocampal lesions only prevent the development of resistance to aversive events when the interval between aversive and subsequent appetitive events exceeds some minimum value.     

Preference for immediate reinforcement over delayed reinforcement: relation between delay discounting and health behavior

Reinforcement from engaging in health behaviors is often delayed by several months or years, a circumstance partly responsible for some people’s increased preference for engaging in unhealthy behaviors associated with immediate reinforcement. To examine whether individuals who discount the future engage in fewer health behaviors, 72 young adults completed questionnaires assessing health behaviors and impulsiveness and laboratory-behavioral measures of impulsive decision making. Regression analyses of impulsivity measures predicting health behavior were only significant for one measure, the Experiential Discounting Task, a task in which monetary consequences of choice were actually experienced by study participants. Participants who discounted most by delay (i.e., exhibited impulsive choice) engaged in fewer health behaviors than those who showed less impulsive responding. This task, in contrast to a hypothetical choice task or self-reported impulsiveness, measures the actual behavior of discounting by delay, and was the facet of impulsive decision making most closely associated with adopting a range of health behaviors.     

Opiate receptors, food intake and obesity

The present studies tested the effect of acute and chronic administration of naloxone on food intake of lean and genetically obese (ob/ob) mice. Acute administration of naloxone, a drug which blocks opiate receptors, produced a greater reduction of food intake in obese (ob/ob) mice than in the lean littermates. For chronic experiments with naloxone, the daily feeding period was shortened to eight hours and two injections of naloxone were given four hours apart. With this procedure of scheduled-feeding the food intake of both lean and obese mice was depressed during the first hour after injecting naloxone. However, beginning on the second day of treatment, the lean mice began to eat more food than the untreated controls during the eight hour feeding period. Food consumption by lean mice reached values 140 to 200% above the control levels between the fourth and sixth day. In the obese mice the rise in food intake was more gradual and did not reach 200% of the control value until the sixth day. Body weight changes reflected the changes in food intake. In contrast to naloxone, chronic treatment with morphine lowered food intake and blocked the stimulatory effect of naloxone. Our findings suggest that endogenous opioids may play a role in signalling satiety and in regulating long-term energy balance.     

The neural substrates responsible for how trait anxiety affects delay discounting: Right hippocampal and cerebellar connectivity with bistable right inferior parietal lobule

Delay discounting, an indicator of impulsivity, refers to the extent of devaluing future rewards. Studies have found that individuals with trait anxiety generally depreciate the later larger rewards, showing steeper delay discounting rates. However, little is known about the neural substrates responsible for how trait anxiety affects individuals' delay discounting. To address this question, we employed the voxel-based morphometry (VBM) and resting-state functional connectivity (RSFC) methods to explore the neural substrates of trait anxiety responsible for delay discounting. Behavioral results showed that trait anxiety was significantly positively correlated with delay discounting rates. The VBM analysis revealed that gray matter volumes of the right hippocampus (RHPC) and right cerebellum (RCere) were significantly positively correlated with trait anxiety. Moreover, the RSFC results showed that bistable right inferior parietal lobule (RIPL) connectivity with the RHPC and RCere were all inversely associated with trait anxiety. More importantly, mediation analysis indicated that trait anxiety played a completely mediating role in the relation between functional connectivity of RHPC-RIPL and RCere-RIPL and delay discounting. These results suggested that bistable RIPL connectivity with RHPC and RCere could be neural substrates underlying the effect of trait anxiety on delay discounting. On the whole, the current study yields insights into how trait anxiety affects delay discounting and provides a novel account from a neural basis perspective.     

Age, weight and obesity

The western world is facing the consequences of higher standards of medical care and improved living conditions. While people are living longer the prevalence of overweight and obesity is escalating which increases the risk of developing non-communicable diseases. However it must be noted that there is a U shaped relationship between weight and mortality with both under and overweight increasing risk. This review examines possible contributory factors for overweight and obesity in older people: life style, depression, changes in body composition, endocrine alterations, sympathetic tone, oxidative stress and concomitant disease.     

Syndromic obesity with neurodevelopmental delay: Opportunities for targeted interventions

Obesity is a growing public health problem in many developed countries, although similar trends are increasingly being described in some developing nations. The genetic underpinnings of obesity continue to arouse increasing research interests, investigations, and discussions. The recent advances in next generation sequencing technologies have shed some more light on the diverse monogenic and polygenic causes of obesity. Syndromic obesity due to chromosomal or monogenic defects has attendant co-morbidities, which may include neurodevelopmental delays, dysmorphism as well as organ-specific developmental anomalies. An improved understanding of the nature of neurodevelopmental challenges in syndromic obesity may pave the way for personalized dietary and physical activity management approaches. This review article describes the clinical and molecular genetic aspects of obesity-related syndromes and the associated neurodevelopmental disabilities. The potential opportunities for individualized nutrigenomic managements of syndromic obesity are also highlighted.     

Independence of food intake and obesity following ventromedial hypothalamic lesions in the rat

Lesions of the ventromedial nucleus of the hypothalamus that do not cause overeating cause significantly greater accumulations of body fat in male rats maintained on an ad lib diet than in controls. Lesioned rats that overeat show a still greater percentage of body fat. The results indicate that obesity caused by medial hypothalamic lesions can result from both primary metabolic disturbances and overeating; and that experimental obesity consistently results from ventromedial hypothalamic lesions independently of the development of hyperphagia.     

成瘾人群的延迟折扣

从延迟折扣角度考察成瘾人群的选择偏好是成瘾研究的重要课题。研究者以酒精成瘾、尼古丁成瘾、药物成瘾和赌博成瘾四类人群为被试,对成瘾行为与延迟折扣的关系进行了探讨。将来的研究应关注延迟折扣与成瘾行为间的作用机制、成瘾人群的延迟折扣效应以及延迟折扣的临床价值等问题。     

Food and addiction among the ageing population

Obesity among the elderly is a growing public health concern. Among the various factors that may contribute to the current rates of obesity is the rewarding aspect of highly palatable foods and beverages, which may lead to overconsumption and excess caloric intake. The present review describes recent research supporting the hypothesis that, for some individuals, the consumption these highly palatable foods and beverages may lead to the development of addictive-like behaviors. In particular, the authors consider the relevance of this hypothesis to the ageing population.     

Self-regulation and obesity: the role of executive function and delay discounting in the prediction of weight loss

Obesity rates are rising worldwide. Executive function and delay discounting have been hypothesized to play important roles in the self-regulation of behavior, and may explain variance in weight loss treatment success. First, we compared individuals with obesity (n?=?82) to healthy weight controls (n?=?71) on behavioral and self-report measures of executive function (working memory, inhibition and shifting) and delay discounting. Secondly, the individuals with obesity took part in a multidisciplinary weight loss program and we examined whether executive function and delay discounting predicted weight change. Individuals with obesity displayed weaker general and food-specific inhibition, and weaker self-reported executive function. Better behavioral working memory and better self-reported inhibition skills in daily life were predictive of greater weight loss. As findings are correlational, future studies should investigate the causal relationship between executive function and weight loss, and test whether intervening on executive function will lead to better prevention and treatment of obesity.     

Variety in the diet enhances intake in a meal and contributes to the development of obesity in the rat

Male and female rats were given three palatable, high energy foods either simultaneously or in succession during three 40 min courses. Both simultaneous and successive variety enhanced energy intake compared to the intake of single palatable foods, which was itself enhanced compared to the intake of chow. Rats deprived of food for 24 hr showed a compensatory increase in chow intake (84%) but only a 20% increase in intake in the single palatable food conditions, and no increase in the variety conditions. Male and female rats showed a similar response to variety and deprivation. The effect of variety on body weight was also examined in rats offered either chow, or chow and one palatable food, or chow and three palatable foods in succession (changed every 12 hr) or simultaneously, for seven weeks. All rats offered the palatable foods were hyperphagic compared to chow-fed controls. Rats given the simultaneous but not the successive variety diet were more hyperphagic than the other palatable food groups and showed significantly greater body weight and fat gains. The availability of a variety of foods is an important factor in the amount eaten in the meal and in the etiology of obesity.     

Olfactory bulb lesions: nest reinforcement and handling reactivity in hamsters

Olfactory bulb lesions in female hamsters were found to alter bar-pressing for nest paper, nest building, bar-pressing for sucrose pellets, stacking of food pellets, maintenance of urination and defecation posts, and handling reactivity. The obtained deficits are interpreted in terms of a sensory deficit related to potentiation of neural mechanisms mediating normal species typical housekeeping activities.     

Differential heart rate responses to social and monetary reinforcement in women with obesity

Obesity is often accompanied by weight stigmatization; subsequently, individuals with obesity frequently face social rejection. It has been shown that recurrent negative social experiences can alter the perception of social cues. However, the way individuals with obesity process social stimuli is not well understood. This study aims to investigate obesity‐related alterations in social compared to nonsocial information processing. Women with obesity (n = 14) and without obesity (n = 14) participated in a social and a monetary incentive delay task in which they anticipated and received positive, negative, and neutral outcomes in the form of faces or money. During the experiment, phasic heart rate changes and reaction times were measured. Women with obesity, compared to lean women, exhibited a stronger differentiation during the anticipation of monetary and social reinforcement, showing slower reaction times to social cues compared to monetary cues. During the outcome processing phase, women with obesity relative to controls demonstrated diminished heart rate responses particularly to negative social outcomes. Interestingly, differences in cardiac responses in participants with obesity were moderated by weight‐related teasing experiences. In women with obesity, a higher BMI was associated with blunted cardiac responses to social cues relative to monetary cues only if they reported more emotional pain after weight‐related teasing. Our results contribute to a better understanding of social information processing in obesity and give first evidence for the role of negative social experiences in reinforcement processing.     

瘦素（leptin）与肥胖

Obesity is a severely public health problem the whole society faces, and it is correlated closely with many diseases, such as diabetesⅡ, hypertension, coronary heart disease,gallqtone, and so on.Therefore it threatens people‘ s survival quality severely. Obesity is a multiple - factor disease including genetic, metabolic and behavioral factor, and the gene is the main determining factor. With the development of molecular biology technique, people have founded several genes involved in obesity. Among these genes, the research on obese gene is the most profound. The protein leptin is the expression product of the obese gene.This review elucidates the structure, the main biological function, the mechanism of leptin and it‘‘s relationship with obesity.     

Relationship between obesity,weight loss,and taste responsiveness

Obese, mildly overweight and normal weight females rated glucose solutions of increasing concentrations for perceived intensity and pleasantness. Obese and mildly overweight subjects found increasingly sweet solutions more pleasant than did normals. Weight loss by dieting did not affect this relationship. Weight loss due to intestinal bypass surgery altered ratings of the pleasantness of glucose solutions, making them appear more similar to ratings given by normal weight individuals. Finally, after weight loss by dieting, all weight groups found the sweet taste of milkshake pleasant even after a preload and consumed large amounts of the milkshake. Prior to weight loss, ingestion of a preload had produced lowered pleasantness ratings and reduced consumption.     

Melatonin and estradiol effects on food intake, body weight, and leptin in ovariectomized rats

OBJECTIVE: The study in ovariectomized (Ovx) rats, as a model of menopausal status, of the effects of melatonin (M) and/or estradiol (E), associated or not with food restriction, on body weight (BW) and serum leptin levels. METHODS: Female SD rats (200-250 g) were Ovx and treated with E, M, E+M or its diluents. Control sham-Ovx rats were treated with E-M diluents. After 7 weeks being fed ad libitum, the animals were exposed for 7 more weeks to a 30% food restriction. We measured: food intake, BW, nocturnal and diurnal urinary excretion of sulphatoxymelatonin (aMT6s), leptin in midday and midnight blood samples, glucose, total cholesterol, LDL, HDL and triglycerides. RESULTS: Day/night rhythm of aMT6s excretion was preserved in all cases. The increase of aMT6s excretion in M-treated animals basically affected the nocturnal period. In animals fed ad libitum, E fully prevented Ovx-induced increase of BW, leptin and cholesterol. Melatonin reduced food intake and partially prevented the increase of BW and cholesterol, without changing leptin levels. Under food restriction, M was the most effective treatment in reducing BW and cholesterol. Leptin levels were similar in M, E or E+M treated rats, and lower than in untreated Ovx rats. CONCLUSIONS: Our result gives a preliminary experimental basis for a post-menopausal co-treatment with estradiol and melatonin. It could combine the effectiveness of estradiol (not modified by melatonin) with the positive effects of melatonin (improvement of sleep quality, prevention of breast cancer, etc.). The possible beneficial effects of melatonin which could justify its use, need to be demonstrated in clinical trials.