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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The behavioral consequences of the central administration of corticotropin releasing hormone (CRH) in rhesus monkeys was determined using food-maintained behavior. Acute doses of CRH (0.003 ng/kg-10 micrograms/kg, i.c.v.), decreased responding for food in a dose- and time-related manner. With intermediate doses, responding occurred at a high rate until food was delivered, and then abruptly ceased for several minutes. Previous studies have attributed similar effects to the noxious properties of certain drugs. Acute doses had no effect on home cage food consumption, body weight, or responding for food on subsequent days. When CRH was given repeatedly for several days, its behavioral suppressant effects increased. Home cage food intake, body weight, and subsequent responding for food decreased for up to 6 weeks before returning to normal. These results suggest that sustained elevations in central levels of CRH can result in a sensitization to its anorexigenic effects, an effect that has not been reported in other species. Because hyperaroused clinical states such as depression and anorexia nervosa are characterized biochemically by hypercortisolism and elevated CRH in CSF, these anorexigenic effects may corroborate a potential role for CRH in affective disorders.
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PMID:Corticotropin releasing hormone produces profound anorexigenic effects in the rhesus monkey. 204 89

The activity anorexia syndrome is characterized by reduced food intake and body weight compared to control levels and increasing levels of physical activity. To induce it, food-restricted rats are confined in running wheels except during the daily meal. We tested whether activity in a flat circular alley also produces the activity anorexia syndrome. In Experiment 1, food-restricted rats were maintained in alleys, wheels, or home cages (control condition). In Experiment 2, they were maintained in alleys, wheels, novel cages, or home cages. The novel cage was added to control for the possibility that the alley might produce an anorectic effect simply because it was a new living space. The alley did not produce the activity anorexia syndrome whereas the wheel did. Although weight loss was greater in the alley than home-cage condition, the alley produced weak, inconsistent suppression of feeding. Moreover, the suppression produced by the alley may have stemmed simply from living in a novel environment. Finally, in contrast to wheel running, alley activity decreased over days. Alley activity, unlike wheel running, may not be reinforcing. Likely, a physical activity must be reinforcing to produce the activity anorexia syndrome. Implications for anorexia nervosa were discussed.
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PMID:Activity in the circular alley does not produce the activity anorexia syndrome in rats. 1074 4

Activity-based anorexia (ABA) is considered an animal model of anorexia nervosa. In ABA, scheduled feeding in combination with voluntary wheel running leads to hyperactivity, reduced food intake, severe body weight loss and hypothermia. In this study it was investigated whether hyperactivity in ABA could be reduced by introducing a warm plate (which was voluntary accessible and did not influence ambient temperature) into a part of the cage. In ad libitum fed rats, the presence of the warm plate did not influence body temperature, running wheel activity (RWA), body weight or food intake. During ABA, however, rats preferred the warm plate and hypothermia was prevented, while hyperactivity and body weight loss were significantly reduced when compared to ABA rats without a plate. Correlation analysis revealed a significant association between basal body temperature and RWA during the light phase in ABA rats. However, there was no evidence that initiation of light phase RWA was a result of hypothermia. These data suggest that ABA rats prefer to prevent hypothermia passively by choosing a warm plate rather than actively regulating body temperature by hyperactivity.
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PMID:Voluntary access to a warm plate reduces hyperactivity in activity-based anorexia. 1592 12

Stress pathologies such as depression and eating disorders (i.e. anorexia nervosa) are associated with amygdalar dysfunction, which are linked with hypothalamic-pituitary-adrenal axis (HPA) axis hyperactivity. The medial amygdaloid nucleus (MeA), a key output nucleus of the amygdaloid complex, promotes HPA axis activation to acute psychogenic stress and is in a prime position to mediate the deleterious effects of chronic stress on physiology and behaviour. The present study tests the hypothesis that the MeA is necessary for the development of maladaptive physiological changes caused by prolonged stress exposure. Male rats received bilateral ibotenate or sham lesions targeting the MeA and one half underwent 2 weeks of chronic variable stress (CVS) or served as home cage controls. Sixteen hours post CVS, all animals were exposed to an acute restraint challenge. CVS induced thymic involution, adrenal hypertrophy, and attenuated body weight gain and up-regulation of hypothalamic corticotrophin-releasing hormone mRNA expression. Consistent with previous literature, lesions of the MeA dampened stress-induced increases in corticosterone after 30 min of exposure to acute restraint stress. However, this effect was independent of CVS exposure, suggesting that the MeA may not be critical for modulating neuroendocrine responses after chronic HPA axis drive. Interestingly, lesion of the MeA modestly exaggerated the stress-induced attenuation of weight gain. Overall, the data obtained suggest that the MeA modulates the neuroendocrine responses to acute but not chronic stress. In addition, the data suggest that the MeA may be an important neural component for the control of body weight in the face of chronic stress.
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PMID:The medial amygdala modulates body weight but not neuroendocrine responses to chronic stress. 1991 76

Anorexia nervosa (AN) is an eating disorder characterized by self-imposed severe starvation and often linked with excessive exercise. Activity-based anorexia (ABA) is an animal model that reproduces some of the behavioral phenotypes of AN, including the paradoxical increase in voluntary exercise following food restriction (FR). Although certain rodents have been used successfully in this animal model, C57BL/6 mice are reported to be less susceptible to ABA. We re-examined the possibility that female C57BL/6 mice might exhibit ABA vulnerability during adolescence, the developmental stage/sex among the human population with particularly high AN vulnerability. After introducing the running wheel to the cage for 3 days, ABA was induced by restricting food access to 1h per day (ABA1, N=13) or 2 h per day (ABA2, N=10). All 23 exhibited increased voluntary wheel running (p<0.005) and perturbed circadian rhythm within 2 days. Only one out of five survived ABA1 for 3 days, while 10 out of 10 survived ABA2 for 3 days and could subsequently restore their body weight and circadian rhythm. Exposure of recovered animals to a second ABA2 induction revealed a large range of vulnerability, even within littermates. To look for the cellular substrate of differences in vulnerability, we began by examining synaptic patterns in the hippocampus, a brain region that regulates anxiety as well as plasticity throughout life. Quantitative EM analysis revealed that CA1 pyramidal cells of animals vulnerable to the second ABA2 exhibit less GABAergic innervation on cell bodies and dendrites, relative to the animals resilient to the second ABA (p<0.001) or controls (p<0.05). These findings reveal that C57BL/6J adolescent females can be used to capture brain changes underlying ABA vulnerability, and that GABAergic innervation of hippocampal pyramidal neurons is one important cellular substrate to consider for understanding the progression of and resilience to AN.
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PMID:Adolescent female C57BL/6 mice with vulnerability to activity-based anorexia exhibit weak inhibitory input onto hippocampal CA1 pyramidal cells. 2352 48

Anorexia nervosa is a debilitating eating disorder characterized by hypophagia, body weight loss, amenorrhea and intense fear of weight gain. In present study, the effect of subchronic agmatine treatment on development of activity based anorexia (ABA) in female rats has been investigated. Animals were injected with saline or agmatine (10-40 mg/kg, ip) just before the onset of dark phase and shifted to experimental cage with wheel for ABA test for 10days. A pre-weighed quantity of food pellets (10g) was placed daily for a restricted period of only 2h (1700-1900h) and food intake was monitored (g) manually by weighing the leftover food. Rats restricted to ABA paradigm, showed greater wheel running, suppressed food consumption, disrupted estrous cycle and weight loss. On the other hand, subchronic agmatine (10-40mg/kg, ip, for 10days) treatment decreased wheel running activity, pronounced increased in food intake and restored body weights as compared to saline treated animals. Further, agmatine treatment decreased corticosterone levels in ABA rats, thereby stabilizing HPA axis in ABA rats. Subchronic agmatine treatment also prevented the disruptions of estrous cycle. Considering the common resistance of anorexia nervosa to current pharmacotherapy, the preliminary data on reduction of physical activity by agmatine, may have potential therapeutic importance. Thus, the role of agmatine in feeding behavior is likely to provide insight into the circumstances that facilitate treatment in eating disorders like anorexia nervosa.
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PMID:Agmatine attenuates hyperactivity and weight loss associated with activity-based anorexia in female rats. 2578 47

Anorexia nervosa (AN) is a psychiatric illness characterized by excessively restricted caloric intake and abnormally high levels of physical activity. A challenging illness to treat, due to the lack of understanding of the underlying neurobiology, AN has the highest mortality rate among psychiatric illnesses. To address this need, neuroscientists are using an animal model to study how neural circuits may contribute toward vulnerability to AN and may be affected by AN. Activity-based anorexia (ABA) is a bio-behavioral phenomenon described in rodents that models the key symptoms of anorexia nervosa. When rodents with free access to voluntary exercise on a running wheel experience food restriction, they become hyperactive - running more than animals with free access to food. Here, we describe the procedures by which ABA is induced in adolescent female C57BL/6 mice. On postnatal day 36 (P36), the animal is housed with access to voluntary exercise on a running wheel. After 4 days of acclimation to the running wheel, on P40, all food is removed from the cage. For the next 3 days, food is returned to the cage (allowing animals free food access) for 2 hr daily. After the fourth day of food restriction, free access to food is returned and the running wheel is removed from the cage to allow the animals to recover. Continuous multi-day analysis of running wheel activity shows that mice become hyperactive within 24 hr following the onset of food restriction. The mice run even during the limited time during which they have access to food. Additionally, the circadian pattern of wheel running becomes disrupted by the experience of food restriction. We have been able to correlate neurobiological changes with various aspects of the animals' wheel running behavior to implicate particular brain regions and neurochemical changes with resilience and vulnerability to food-restriction induced hyperactivity.
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PMID:Using the Activity-based Anorexia Rodent Model to Study the Neurobiological Basis of Anorexia Nervosa. 2655 18

Hyperactivity is a core symptom in various psychiatric disorders, including attention-deficit/hyperactivity disorder, schizophrenia, bipolar disorders, and anorexia nervosa. Although hyperactivity has been linked to dopaminergic signalling, the causal relationship between midbrain dopamine neuronal activity and locomotor hyperactivity remains unknown. In this study, we test whether increased dopamine neuronal activity is sufficient to induce locomotor hyperactivity. To do so, we used designer receptors exclusively activated by designer drugs (DREADD) to chemogenetically enhance neuronal activity in two main midbrain dopamine neuron populations, i.e. the ventral tegmental area (VTA) and substantia nigra pars compacta (SN), in TH:Cre rats. We found that activation of VTA dopamine neurons induced a pronounced and long-lasting hyperactive phenotype, whilst SN dopamine neuron activation only modestly increased home cage locomotion. Furthermore, this hyperactive phenotype was replicated by selective activation of the neuronal pathway from VTA to the nucleus accumbens (NAC). These results show a clear functional difference between neuronal subpopulations in the VTA and SN with regards to inducing locomotor hyperactivity, and suggest that the dopaminergic pathway from VTA to NAC may be a promising target for the treatment of hyperactivity disorders.
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PMID:Chemogenetic activation of dopamine neurons in the ventral tegmental area, but not substantia nigra, induces hyperactivity in rats. 2771 62