Visual stimuli may play an important role in the development and maintenance of addiction in humans. Research with a visually oriented animal model such as Japanese quail (Coturnix japonica) may provide insight into how visual cues contribute to the addiction process. The aim of the current study was to investigate the rewarding properties of nicotine in male Japanese quail using a biased conditioned place preference (CPP) procedure. Adult male quail (N = 30) were allowed to freely explore the entire CPP apparatus during a place preference pre-test and time spent in each chamber was measured. During nicotine conditioning sessions, quail were administered nicotine (0.5, 1.0, or 2.0 mg/kg) or saline and were then confined to their initially least preferred chamber. On alternating days, all quail received saline and were confined to their initially preferred chamber. Locomotor activity was assessed in both chambers. The conditioning chambers had yellow or green walls to enhance the visual salience of each context. Following 8 conditioning sessions (4 nicotine; 4 saline), quail were allowed to explore the entire apparatus during a CPP post-test and time spent in each chamber was measured. The results indicated that quail treated with 0.5 and 1.0 mg/kg nicotine significantly increased the amount of time they spent in the nicotine-paired chamber compared to saline controls, suggesting that nicotine produced a CPP. Furthermore, quail treated with 0.5 mg/kg nicotine showed a significant increase in locomotor activity with repeated treatments. The current findings suggest that nicotine may have a rewarding effect in quail and may tentatively suggest that the neuropharmacological mechanisms that mediate CPP for nicotine are conserved in birds.
Nicotine; CPP; Avian; Visual cues; Drug Reward
Physiological and nutritional state can modify sensory ability and perception through hormone signaling. Obesity and related metabolic disorders present a chronic imbalance in hormonal signaling that could impact sensory systems. In the olfactory system, external chemical cues are transduced into electrical signals to encode information. It is becoming evident that this system can also detect internal chemical cues in the form of molecules of energy homeostasis and endocrine hormones, whereby neurons of the olfactory system are modulated to change animal behavior towards olfactory cues. We hypothesized that chronic imbalance in hormonal signaling and energy homeostasis due to obesity would thereby disrupt olfactory behaviors in mice. To test this idea, we utilized three mouse models of varying body weight, metabolic hormones, and visceral adiposity – 1) C57BL6/J mice maintained on a condensed-milk based, moderately high-fat diet (MHF) of 32% fat for 6 months as the diet-induced obesity model, 2) an obesity-resistant, lean line of mice due to a gene-targeted deletion of a voltage-dependent potassium channel (Kv1.3-null), and 3) a genetic model of obesity as a result of a gene-targeted deletion of the melanocortin 4 receptor (MC4R-null). Diet-induced obese (DIO) mice failed to find fatty-scented hidden peanut butter cracker, based solely on olfactory cues, any faster than an unscented hidden marble, initially suggesting general anosmia. However, when these DIO mice were challenged to find a sweet-scented hidden chocolate candy, they had no difficulty. Furthermore, DIO mice were able to discriminate between fatty acids that differ by a single double bond and are components of the MHF diet (linoleic and oleic acid) in a habituation-dishabituation paradigm. Obesity-resistant, Kv1.3-null mice exhibited no change in scented object retrieval when placed on the MHF-diet, nor did they perform differently than wild-type mice in parallel habituation-dishabituation paradigms of fatty food-related odor components. Genetically obese, MC4R-null mice successfully found hidden scented objects, but did so more slowly than lean, wild-type mice, in an object-dependent fashion. In habituation-dishabituation trials of general odorants, MC4R-null mice failed to discriminate a novel odor, but were able to distinguish two fatty acids. Object memory recognition tests for short- and long-term memory retention demonstrated that maintenance on the MHF diet did not modify ability to perform these tasks independent of whether mice became obese or were resistant to weight gain (Kv1.3-null), however, the genetically predisposed obese mice (MC4R-null) failed the long-term object memory recognition performed at 24 hours. These results demonstrate that even though both the DIO mice and genetically predisposed obese mice are obese, they vary in the degree to which they exhibit behavioral deficits in odor detection, odor discrimination, and long-term memory.
olfactory; cognition; memory; obese; diet-induced obesity; Kv1.3
Alcohol dependence in aging populations is seen as a public health concern, most recently because of the significant proportion of heavy drinking among “Baby Boomers.” Basic animal research on the effects of aging on physiological and behavioral regulation of ethanol (EtOH) intake is sparse, since most of this research is limited to younger models of alcoholism. Here, EtOH drinking and preference were measured in groups of aged Syrian hamsters. Further, because voluntary exercise (wheel-running) is a rewarding substitute for EtOH in young adult hamsters, the potential for such reward substitution was also assessed.
Aged (24 month-old) male hamsters were subjected to a three-stage regimen of free-choice EtOH (20% v/v) or water and unlocked or locked running wheels to investigate the modulatory effects of voluntary wheel running on EtOH intake and preference. Levels of fluid intake and activity were recorded daily across 60 days of experimentation.
Prior to wheel running, levels of EtOH intake were significantly less than levels of water intake, resulting in a low preference for EtOH (30%). Hamsters with access to an unlocked running wheel had decreased EtOH intake and preference compared with hamsters with access to a locked running wheel. These group differences in EtOH intake and preference were sustained for up to 10 days after running wheels were re-locked.
These results extend upon those of our previous work in young adult hamsters, indicating that aging dampens EtOH intake and preference. Voluntary wheel running further limited EtOH intake, suggesting that exercise could offer a practical approach for managing late-life alcoholism.
Considerable evidence implicates the endocannabinoid system as a neuromodulator of nausea and vomiting. The action of anandamide (AEA) can be prolonged by inhibiting its degradation, through the use of URB597 (URB), a Fatty Acid Amide Hydrolase (FAAH) enzyme inhibitor. Here we present evidence that the FAAH inhibitor, URB, interferes with cisplatin- and nicotine -induced vomiting in the Suncus murinus. In Experiment 1, shrews were injected with URB (0.9 mg/kg) or vehicle 120 min prior to the behavioral testing. They received a second injection of AEA (5 mg/kg) or vehicle 15 min prior to being injected with cisplatin (20 mg/kg) or saline and the number of vomiting episodes were counted for 60 min. In Experiment 2, shrews were injected with vehicle or URB (0.9 mg/kg) 120 min prior to receiving an injection of nicotine (5 mg/kg) or saline and the number of vomiting episodes were counted for 15 min. Experiment 3 evaluated the potential of the CB1 antagonist, SR141716, to reverse the effect of URB on nicotine-induced vomiting. URB attenuated vomiting produced by cisplatin and nicotine and the combination of URB+AEA suppressed vomiting produced by cisplatin. The effect of URB on nicotine-induced vomiting was reversed by SR141716. These data suggest that the EC system plays a tonic role in the regulation of toxin-induced vomiting.
Emesis; Endocannabinoid; shrew; FAAH; Nicotine; Cisplatin
We recently reported that the latency to begin drinking water during slow, intravenous infusion of a concentrated NaCl solution was shorter in estradiol-treated ovariectomized rats compared to oil vehicle-treated rats, despite comparably elevated plasma osmolality. To test the hypothesis that the decreased latency to begin drinking is attributable to enhanced detection of increased plasma osmolality by osmoreceptors located in the CNS, the present study used immunocytochemical methods to label fos, a marker of neural activation. Increased plasma osmolality did not activate the subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), or the nucleus of the solitary tract (NTS) in either oil vehicle-treated ratsor estradiol-treated rats. In contrast, hyperosmolality increased fos labeling in the area postrema (AP), the paraventricular nucleus of the hypothalamus (PVN) and the rostral ventrolateral medulla (RVLM) in both groups; however, the increase was blunted in estradiol-treated rats. These results suggest that estradiol has selective effects on the sensitivity of a population of osmo-/Na+-receptors located in the AP, which, in turn, alters activity in other central areas associated with responses to increased osmolality. In conjunction with previous reports that hyperosmolality increases blood pressure and that elevated blood pressure inhibits drinking, the current findings of reduced activation in AP, PVN, and RVLM–areas involved in sympathetic nerve activity–raise the possibility that estradiol blunts HS-induced blood pressure changes. Thus, estradiol may eliminate or reduce the initial inhibition of water intake that occurs during increased osmolality, and facilitate a more rapid behavioral response, as we observed in our recent study.
Circumventricular organs; Area postrema; Paraventricular nucleus; Rostral ventrolateral medulla; Nucleus of the solitary tract; Osmolality
In the last decade, the neurologic effects of various air pollutants have been the focus of increasing attention. The main purpose of this study was to assess the potential impact of early childhood exposure to indoor molds on the subsequent cognitive function of 6-year old children. The results of this study are based on the six-year follow-up of 277 babies born at term to mothers participating in a prospective cohort study in Krakow, Poland. The study participants are all non-smoking pregnant women who were free of chronic diseases such as diabetes and hypertension.
The presence of visible mold patches on indoor walls was monitored at regular time intervals over gestation and after birth up to the age of five. The Wechsler Intelligence Scale for Children (WISC-R) was administered to children at age 6. The exposure effect of living in mold-contaminated homes on the IQ scores of children was adjusted for major confounders, known to be important for the cognitive development of children such as maternal education, the child’s gender, breastfeeding practices in infancy, the presence of older siblings and the prenatal exposure to lead and environmental tobacco smoke (ETS).
The adjusted IQ deficit attributed to longer exposures to indoor molds (> 2 years) was significantly lower on the IQ scale (beta coeff. = −9.16, 95%CI: −15.21, −3.10) and tripled the risk of low IQ scoring (OR= 3.53; 95%CI: 1.11 – 11.27) compared with references. While maternal education (beta coeff. = 0.61, 95%CI: 0.05, 1.17) and breastfeeding (beta coeff. = 4.0; 95%CI: 0.84, 7.17) showed a significant positive impact on cognitive function, prenatal ETS exposure (beta coeff. = −0.41; 95%CI: −0.79, −0.03) and the presence of older siblings (beta coefficient= −3.43; 95%CI: −5.67, −1.20) were associated with poorer cognitive function in children.
In conclusion, the results of this study draw attention to the harmful effect of early postnatal exposure to indoor molds on children cognitive development and provide additional evidence on the role of environmental determinants in human cognitive development.
cognitive function; children; exposure to molds; breastfeeding; prospective birth cohort study
Following an acute stressor, pre-adolescent rats exhibit a protracted hormonal response compared to adults, while after repeated exposure to the same stressor (i.e., homotypic stress) prepubertal males fail to habituate like adults. Though the neurobehavioral implications of these changes are unknown, studying pubertal shifts in stress reactivity may help elucidate the mechanisms that underlie the increase in stress-related psychological and physiological disorders often observed during adolescence. Here, we investigated hormonal, behavioral, and neural responses of prepubertal (30d) and adult (77d) male rats before, during, or after acute stress (restraint), homotypic stress (repeated restraint) or heterotypic stress (repeated cold exposure followed by restraint). We found that prepubertal males exhibit prolonged corticosterone responses following acute and heterotypic stress, and higher adrenocorticotropic hormone and corticosterone responses after homotypic stress, compared to adults. Despite these significant age-dependent changes in hormonal responsiveness, we found struggling behavior during restraint was similar at both ages, such that both prepubertal and adult animals exposed to homotypic stress struggled less than animals exposed to either acute or heterotypic stress. Across these different stress paradigms, we found greater neural activation, as indexed by FOS immunostaining, in the prepubertal compared to adult paraventricular nucleus of the hypothalamus, a nucleus integral for initiating the hormonal stress response. Interestingly, however, we did not find any influence of pubertal development on stress-induced activation of the posterior paraventricular thalamic nucleus, a brain region involved in experience-dependent changes in stress reactivity. Collectively, our data indicate prepubertal and adult males display divergent hormonal, behavioral, and neural responses following a variety of stressful experiences, as well as a distinct dissociation between hormonal and behavioral reactivity in prepubertal males under homotypic conditions.
Acute Stress; Adolescence; Heterotypic Stress; Homotypic Stress; Struggling Behavior
Rats that consume high-energy (HE) diets (i.e., diets high in saturated fats and sugar) show impaired hippocampal-dependent learning and memory (e.g., ). To further investigate this effect, we trained rats given restricted access to low-fat lab chow on hippocampal-dependent serial feature-negative (FN) and hippocampal-independent simple discrimination problems. When training was completed, Group Chow received ad libitum lab chow. The remaining rats received ad libitum HE diet. Performance on both discrimination problems was tested following 7, 14, 21 and 28 days of HE diet exposure. FN, but not simple discrimination, was abolished initially for all rats, and then re-emerged for Group Chow. For rats fed HE diet, those that weighed the least and had lowest amount of body fat (HE-diet resistant (HE-DR) rats), performed like Group Chow on both discrimination problems. However, HE diet-induced obese (HE-DIO) rats (i.e., rats that weighed the most weight and had the most body fat) performed like Group Chow on the simple discrimination problem, but were impaired throughout testing on the FN problem. Subsequent assessment of blood-brain barrier (BBB) permeability revealed that concentrations of an exogenously administered dye were elevated in the hippocampus, but not in the striatum or prefrontal cortex for HE-DIO rats relative to the HE-DR and Chow groups. The results indicate that the adverse consequences of HE diet on hippocampal-dependent cognitive functioning are associated with detrimental effects on the BBB and that both of these outcomes vary with sensitivity to HE diet-induced increases in weight and adiposity.
hippocampus; high-fat diet; obesity; learning; adiposity; energy balance; cognition
The rapid increase in the prevalence of obesity is a priority for investigators from across numerous disciplines, including biology, nutritional science, and public health and policy. In this paper, we systematically examine the premise that common dietary obesity is an addictive disorder, based on the criteria for addiction described in the Diagnostic and Statistical Manual (DSM) of Mental Disorders of the American Psychiatric Association, version IV, and consider the consequences of such a reclassification of obesity for public policy. Specifically, we discuss evidence from both human and animal studies investigating the effects of various types and amounts of food and the food environment in obese individuals. Neurobiological studies have shown that the hedonic brain pathways activated by palatable food overlap considerably with those activated by drugs of abuse and suffer significant deficits after chronic exposure to high-energy diets. Furthermore, food as a stimulus can induce the sensitization, compulsion and relapse patterns observed in individuals who are addicted to illicit drugs. The current food environment encourages these addictive-like behaviors where increased exposure through advertisements, proximity and increased portion sizes are routine. Taking lessons from the tobacco experience, it is clear that reclassifying common dietary obesity as an addictive disorder would necessitate policy changes (e.g., regulatory efforts, economic strategies, and educational approaches). These policies could be instrumental in addressing the obesity epidemic, by encouraging the food industry and the political leadership to collaborate with the scientific and medical community in establishing new and more effective therapeutic approaches.
Hormones associated with pregnancy and parturition have been implicated in facilitating the onset of maternal behavior via reductions in neophobia, anxiety, and stress responsiveness. To determine whether the onset of paternal behavior has similar associations in biparental male California mice (Peromyscus californicus), we compared paternal responsiveness, neophobia (novel-object test), and anxiety-like behavior (elevated plus maze, EPM) in isolated virgins (housed alone), paired virgins (housed with another male), expectant fathers (housed with pregnant pairmate), and new fathers (housed with pairmate and pups). Corticotropin-releasing hormone (CRH) and Fos immunoreactivity (IR) were quantified in brain tissues following exposure to a predator-odor stressor or under baseline conditions. New fathers showed lower anxiety-like behavior than expectant fathers and isolated virgins in EPM tests. In all housing conditions, stress elevated Fos-IR in the hypothalamic paraventricular nucleus (PVN). Social isolation reduced overall (baseline and stress-induced) Fos- and colocalized Fos/CRH-IR, and increased overall CRH-IR, in the PVN. In the central nucleus of the amygdala, social isolation increased stress-induced CRH-IR and decreased stress-induced activation of CRH neurons. Across all housing conditions, paternally behaving males displayed more anxiety-related behavior than nonpaternal males in the EPM, but showed no differences in CRH- or Fos-IR. Finally, the latency to engage in paternal behavior was positively correlated with the latency to approach a novel object. These results suggest that being a new father does not reduce anxiety, neophobia, or neural stress responsiveness. Low levels of neophobia, however, were associated with, but not necessary for paternal responsiveness.
Paternal behavior; stress; CRH; biparental; anxiety; neophobia
We examined the role of T1r3 and Trpm5 taste signaling proteins in carbohydrate-induced overeating and obesity. T1r3, encoded by Tas1r3, is part of the T1r2+T1r3 sugar taste receptor, while Trpm5 mediates signaling for G protein-coupled receptors in taste cells. It is known that C57BL/6 wild-type (WT) and Tas1r3 knock-out (KO) mice are attracted to the taste of Polycose (a glucose polymer), but not sucrose. In contrast, Trpm5 KO mice are not attracted to the taste of sucrose or Polycose. In Experiment 1, we maintained the WT, Tas1r3 KO and Trpm5 KO mice on one of three diets for 38 days: lab chow plus water (Control diet); chow, water and 34% Polycose solution (Polycose diet); or chow, water and 34% sucrose solution (Sucrose diet). The WT and Tas1r3 KO mice overconsumed the Polycose diet and became obese. The WT and Tas1r3 KO mice also overconsumed the Sucrose diet, but only the WT mice became obese. The Trpm5 KO mice, in contrast, showed little or no overeating on the Sucrose and Polycose diets, and gained slightly or significantly less weight than WT mice on these diets. In Experiment 2, we asked whether the Tas1r3 KO mice exhibited impaired weight gain on the Sucrose diet because it was insipid. To test this hypothesis, we maintained the WT and Tas1r3 KO mice on one of two diets for 38 days: chow, water and a dilute (1%) but highly palatable Intralipid emulsion (Control diet); or chow, water and a 34% sucrose + 1% Intralipid solution (Suc+IL diet). The WT and Tas1r3 KO mice both gained weight and became obese on the Suc+IL diet. Our results suggest that nutritive solutions must be highly palatable to cause carbohydrate-induced obesity in mice, and that palatability produces this effect in part by enhancing nutrient utilization.
palatability; taste; carbohydrate; diet-induced obesity; nutrient utilization
Both animals and humans show a tendency toward eating more “comfort food” (high fat, sweet food) after acute stress. Such stress eating may be contributing to the obesity epidemic, and it is important to understand the underlying psychobiological mechanisms. Prior investigations have studied what makes individuals eat more after stress; this study investigates what might make individuals eat less. Leptin has been shown to increase following a laboratory stressor, and is known to affect eating behavior. This study examined whether leptin reactivity accounts for individual differences in stress eating. To test this, we exposed forty women to standardized acute psychological laboratory stress (Trier Social Stress Test) while blood was sampled repeatedly for measurements of plasma leptin. We then measured food intake after the stressor in 29 of these women. Increasing leptin during the stressor predicted lower intake of comfort food. These initial findings suggest that acute changes in leptin may be one of the factors modulating down the consumption of comfort food following stress.
Prenatal exposure to alcohol may exert a significant detrimental effect on the functioning of the individual’s brain, however few studies have examined this before birth. This longitudinal study examined the effect of maternal alcohol consumption on the elicited startle response of the fetus. Two groups of fetuses were examined: one whose mothers drank alcohol (approximately 10 units per week); the other whose mothers did not drink alcohol. Fetuses were examined at 29, 32 and 35 weeks gestation and their startle response observed using ultrasound in response to 2 presentations of a pink noise (70–250Hz) at 90dB(A) separated by 30 seconds. Fetuses exposed to alcohol exhibited a weaker startle response at 29 weeks gestation than did fetuses not exposed to alcohol. There was no difference in the response at 32 and 35 weeks gestation. To ensure the effects were not due to a more general effect of alcohol on fetal movement, a second experiment compared the spontaneous movements (observed on ultrasound for 45 minutes) of fetuses whose mothers drank alcohol and fetuses of mothers who didn’t drink alcohol. There were no differences in movements exhibited by the fetuses. The results suggest that exposure to alcohol delays the emergence of the elicited startle response at 29 weeks gestation but this delay has disappeared by 32 weeks gestation. The possible role of altered neural development, acute exposure to alcohol and disruptions to the fetus’s behavioural repertoire, in mediating these effects are discussed.
Startle; Prenatal; Alcohol; CNS; Neurobehavioural; Fetus
It is well documented that the quality and quantity of prior sleep influences future sleep. For instance, nocturnal sleep restriction leads to an increase in slow wave sleep (SWS) (i.e. SWS rebound) during a subsequent sleep period. However, few studies have examined how prior napping affects daytime sleep architecture. Becuase daytime naps are recommended for management of disrupted sleep, understanding the impact of napping on subsequent sleep may be important. We monitored sleep-wake patterns for one week with actigraphy followed by a 75-minute polysomnographically-recorded nap. We found that greater nap frequency was correlated with increased Stage 1 and decreased SWS. We categorized subjects based on nap frequency during the prior week (0 naps, 1 to 2 naps, and 3 to 4 naps) and found differences in Stage 1, Stage 2, and SWS between groups. Subjects who took no naps had the greatest amount of SWS, those who took 1 to 2 naps had the most Stage 2 sleep, and those who took 3 to 4 naps had the most Stage 1. While correlations were not found between nap frequency and nocturnal sleep measures, frequent napping was associated with increased subjective sleepiness. Therefore, frequent napping appears to be associated with lighter daytime sleep and increased sleepiness during the day. Speculatively, low levels of daytime sleepiness and increased SWS in non-nappers may help explain why these individuals choose not to nap.
Sleep architecture; Napping; Slow Wave Sleep; Sleepiness
Variations in fat preference and intake across humans are poorly understood in part because of difficulties in studying this behavior. The objective of this study was to develop a simple procedure to assess fat discrimination, the ability to accurately perceive differences in the fat content of foods, and assess the associations between this phenotype and fat ingestive behaviors and adiposity. African-American adults (n=317) were tested for fat discrimination using 7 forced choice same/different tests with Italian salad dressings that ranged in fat-by-weight content from 5–55%. Performance on this procedure was determined by tallying the number of trials in which a participant correctly identified the pair of samples as “same” or “different” across all test pairs (ranging from 1–7). Individuals who received the lowest scores on this task (≤3 out of 7 correct) were classified as fat non-discriminators (n=33) and those who received the highest scores (7 out of 7 correct) were classified as fat discriminators (n=59). These 2 groups were compared for the primary outcome variables: reported food intake, preferences, and adiposity. After adjusting for BMI, sex, age, and dietary restraint and disinhibition, fat non-discriminators reported greater consumption of both added fats and reduced fat foods (p<0.05 for both). Fat non-discriminators also had greater abdominal adiposity compared to fat discriminators (p<0.05). Test-retest scores performed in a subset of participants (n=40) showed moderate reliability of the fat discrimination test (rho=0.53;p<0.01). If these results are replicated, fat discrimination may serve as clinical research tool to identify participants who are at risk for obesity and other chronic diseases due to increased fat intake.
oral fat perception; fat intake; obesity
Due to the high prevalence of overweight and obesity, developing strategies to improve weight loss and weight loss maintenance is imperative. One dietary environmental variable that has received little attention in being targeted in an intervention to assist with obesity treatment is dietary variety. Experimental research has consistently shown that greater dietary variety increases consumption, with the effect of variety on consumption hypothesized to be a consequence of the differential experience of the more varied sensory properties of food under those conditions with greater dietary variety. As reduced energy intake is required for weight loss, limiting variety, particularly in food groups that are high in energy-density and low in nutrient-density, may assist with reducing energy intake and improving weight loss. A series of investigations, both observational and experimental, were conducted to examine if limiting variety in an energydense, non-nutrient-dense food group, snack foods (i.e., cookies, chips), assisted with reducing energy intake of the food group and improving weight loss. Results of the investigations suggest that a prescription for limiting variety in a food group can be implemented during obesity treatment, limiting variety is associated with the occurrence of monotony, and that reducing food group variety is related to decreased consumption of that food group. Future research is needed to ascertain the long-term effect of prescriptions targeting dietary variety on weight loss and weight loss maintenance.
Variety; Food group; Energy intake; Weight loss; Monotony
There is emerging evidence that two parallel lines of gustatory information are generated in taste buds. One pathway leads to higher cortical centers and is involved in discriminating basic taste qualities (sweet, bitter, sour, salty, umami) and perceiving flavors. The other pathway may conduct information involved in physiological reflexes such as swallowing, salivation, and cephalic phase digestion. If this notion is true, the existence of two populations of taste bud cells that have different functional characteristics may lie at the origins of the two pathways. This speculative concept is explored in this review of taste signal processing in mammalian taste buds.
Taste transmitters; ATP; Serotonin; 5-HT; Noradrenalin; Pannexin 1; Cephalic phase digestion; Taste receptor cells; Taste bud synapses
The purpose of this study was to test the associations between cognitive and psychological eating behavior traits and detailed measures of adiposity and body fat distribution using imaging-based methods in a cross-sectional study. Eating behavior traits (compensatory and routine restraint, external eating, and emotional eating) were assessed using the validated Weight-Related Eating Questionnaire, and measures of adiposity using anthropometry, dual energy X-ray absorptiometry (DXA), and magnetic resonance imaging (MRI). Each adiposity outcome of interest (total fat, ratio of trunk fat to periphery fat, visceral and subcutaneous fat as % of abdominal area, and % liver fat) was regressed on the four eating behaviors while adjusting for age and race/ethnicity. This study included a total of 60 postmenopausal Japanese American (n=30) and white (n=30) women (age: 60-65y, BMI: 18.8-39.6 kg/m2). Weight-related eating behavior traits did not differ by ethnicity. Higher external eating scores were associated with measures of total adiposity, including higher BMI (β = 0.36, p = 0.02) and DXA total fat mass (β = 0.41, p = 0.001), and with MRI abdominal subcutaneous fat (β = 0.55, p = 0.001). Higher routine restraint scores were associated with visceral adiposity (β = 0.42, p = 0.04). Our findings suggest that different weight-related eating behavior traits might increase not only total adiposity but also abdominal and visceral fat deposition associated with higher metabolic risks. Future research, preferably in a prospective study of men and women and including biomarkers related to psychological stress, will be needed to explore potential underlying biological mechanisms.
Eating Behaviors; Body Fat Distribution; Central Obesity; Liver Fat; Subcutaneous Adipose Tissue; Visceral Fat
The traditional approach to the study of thermoregulation in young animals focuses on the regulatory capacities of individuals, which, for multiparous species, risks ignoring critical aspects of the early developmental niche. Here, we examined the ontogeny of regulatory behavior in C57BL/6 mice, employing simultaneous behavioral, thermographic, and acoustic measures of groups and individual pups. Litters of mice were placed in a chamber on Postnatal Day (PND) 2, 4, or 8, in which the ambient temperature (Ta) gradually cycled (over 50 min) from warm (36.5°C) to cool (20°C) and back (to 36.5°C). Litters of all three ages displayed “group regulatory behavior,” whereby group size varied with changes in Ta. This coupling, moreover, improved with age. Infrared thermography was used to monitor skin temperature of pups’ interscapular (TIS) and rump (Trump) areas, and to estimate brown adipose tissue (BAT) thermogenesis (TIS − Trump) in PND4 and PND8 individuals and huddles. Huddling was found to significantly reduce heat loss in pups subject to thermal challenge as groups, compared to pups challenged as individuals. Additionally, females were found to display significantly warmer TIS and Trump values than male huddlemates. Huddling did not have a consistent effect on emissions of ultrasonic vocalizations, which were generally correlated with ambient temperature and BAT activation. Our results indicate that simultaneous measures of behavioral and physiological response to cooling may prove useful for a variety of applications, including the phenotyping of social dysfunction.
Huddling; Brown adipose tissue; ultrasonic vocalization; thermoregulation; behavioral phenotyping; C57BL/6
The objective of this study was to determine whether humans could detect long-chain fatty acids when these lipid molecules are delivered to the oral cavity by edible taste strips. For suprathreshold studies, up to 1.7 umoles of stearic acid or linoleic acid were incorporated into 0.03 mm thick, one-inch square taste strips. Normalized taste intensity values for stearic acid were in the barely detectable range, with values equal to, or slightly above control strips. One-third of test subjects described the taste quality as oily/fatty/waxy. Approximately 75% of test subjects could detect the presence of linoleic acid when this fatty acid was incorporated into dissolvable strips. Normalized taste intensity values for linoleic acid were in the weak to moderate range. The most commonly reported taste quality responses for linoleic acid were fatty/oily/waxy, or bitter. When nasal airflow was obstructed, the perceived taste intensity of linoleic acid decreased by approximately 40 percent. Taste intensity values and taste quality responses for linoleic acid were then compared among tasters and non-tasters of 6-n-propylthiouracil (PROP). Individuals who could detect the bitter taste of PROP reported higher taste intensity values for linoleic acid compared with PROP non-tasters. However, taste quality responses for linoleic acid were similar among both PROP tasters and PROP non-tasters. These results indicate that humans can detect long-chain fatty acids by both olfactory and non-olfactory pathways when these hydrophobic molecules are delivered to the oral cavity by means of edible taste strips. These studies further show that genetic variation in taste sensitivity to PROP affects chemosensory responses to the cis-unsaturated fatty acid linoleic acid in the oral cavity.
Most studies agree that males and females respond differently to drugs of abuse. In females, estradiol enhances the behavioral response to cocaine. However, studies on the role of testosterone and the locomotor response to psychostimulants in the male rat are inconclusive. Our study was designed to determine the behavioral effects of testosterone on the development and persistence of cocaine sensitization in male rats. We tested different doses of cocaine (10, 15 and 30mg/kg) to determine which dose induced locomotor sensitization in intact (INT) and gonadectomized (GDX) animals. We also investigated if GDX males with testosterone replacement (GDX-T) showed a similar locomotor response to cocaine as INT males.
Our data showed that gonadectomy enhanced the locomotor response to a single cocaine injection. This effect was not observed in gonadectomized rats that received testosterone replacement. However, GDX rats did not show a progressive increase in their locomotor response to repeated cocaine administration (15 and 30 mg/kg) (sensitization) as did INT and GDX-T animals. It is possible that in GDX males, the initial high locomotor response to cocaine creates a ceiling effect that limits further increase in cocaine-induced hyperactivity. These findings indicate that testosterone not only modulates the behavioral response to a single and to repeated cocaine injections, but is essential for male rats to become sensitized to cocaine.
Gonadectomy; Testosterone; Cocaine; Behavioral Sensitization; Locomotor Activity; Castration; Dose Response
Although partially controlled with antiemetic drugs, postoperative nausea and vomiting (PONV) continues to be a problem for many patients. Clinical research suggests that opioid analgesics and volatile anesthetics are the main triggers of PONV. The aim of this study was to develop an animal model for post-anesthesia vomiting for future studies to further determine mechanisms and preclinical drug efficacy. Ferrets (N=34) were initially used because they have served as a gold standard for emesis research. Ferrets were tested with several doses of morphine, inhaled isoflurane, and a positive control injection of cisplatin (a chemotherapy agent) to induce emesis. Musk shrews (a small animal model; N=36) were also tested for emesis with isoflurane exposure. A control injection of cisplatin produced emesis in ferrets (ip, 129.8±22.0 retches; 13.7±2.3 vomits; mean ± SEM). Morphine produced a dose-response on emesis in ferrets, with maximal responses at 0.9 mg/kg (sc, 29.6±12.6 retches; 1.8±0.9, vomits). Isoflurane exposure (2–4% for 10 min to 6 h exposure) failed to induce vomiting, was not associated with an increased frequency in emesis when combined with a low dose of morphine (0.1 mg/kg, sc), and failed to produced consistent effects on food and water intake. In contrast to ferrets, musk shrews were very sensitive to isoflurane-induced emesis (0.5 to 3%, 10 min exposure; up to 11.8±2.4 emetic episodes). Overall, these results indicate that ferrets will not be useful for delineating mechanisms responsible for isoflurane-induced emesis; however, musk shrews may prove to be a model for vomiting after inhalation of volatile agents.
Vomiting; Nausea; Models; Animal; Behavior
Taste neophobia is manifested behaviorally as lower intake of a novel, potentially dangerous tastant relative to the same tastant when it is perceived as safe and familiar. To further characterize this phenomenon, microstructural analysis of lick patterns was used to track the transition from novel to familiar for three tastants: saccharin, quinine and Polycose. The results revealed that in addition to an increase in the amount consumed (for saccharin and quinine but not Polycose), cluster size (an index of palatability) became larger as familiarity with the benign tastants increased. The current finding suggests that the pleasure of drinking increases as the novel, potentially dangerous tastant becomes accepted as safe.
Novelty; Danger; Microstructural lick analysis; Post-ingestive feedback; Rat
There has been scant work to investigate the mechanisms influencing macronutrient selection by mice. Here, we measured the consumption and choice of carbohydrate- and fat-containing diets by NZW/LacJ (NZW) and BTBR/T+ tf/J (BTBR) strains. We found that NZW mice voluntarily ate more carbohydrate and less fat than did BTBR mice. Mice with a BTBR background and a heterozygous (BTBR/NZW) congenic region on chromosome 17 between 25.7 – 27.5 Mb (N10 generation) or 26.7 – 27.5 Mb (N12 generation) also ate more carbohydrate and less fat than did homozygous (BTBR/BTBR) littermate controls. Of the 21 known and predicted genes in the congenic interval between 26.7 – 27.5 Mb, we raise for consideration as a causative candidate Itpr3, the inositol triphosphate receptor type 3 gene, which is a component of the GPCR-mediated taste transduction cascade. We speculate that a mutation in Itpr3 influences food choice by impairing the detection of nutrients in the macronutrient-containing diets.
Carbohydrate intake; fat intake; diet selection; taste preferences
Glucagon-like peptide-1 (GLP-1) is released in response to nutrient ingestion and is a regulator of energy metabolism and consummatory behaviors through both peripheral and central mechanisms. The GLP-1 receptor (GLP-1R) is widely distributed in the central nervous system, however little is known about how GLP-1Rs regulate ambulatory behavior. The abused psychostimulant amphetamine (AMPH) promotes behavioral locomotor activity primarily by inducing the release of the neurotransmitter dopamine. Here, we identify the GLP-1R agonist exendin-4 (Ex-4) as a modulator of behavioral activation by AMPH. We report that in rats a single acute administration of Ex-4 decreases both basal locomotor activity as well as AMPH-induced locomotor activity. Ex-4 did not induce behavioral responses reflecting anxiety or aversion. Our findings implicate GLP-1R signaling as a novel modulator of psychostimulant-induced behavior and therefore a potential therapeutic target for psychostimulant abuse.
amphetamine; psychostimulant; Glucagon-like peptide-1; exenatide; dopamine