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This study aims to evaluate the impact of neonatal arthritis on adult pain threshold, sleep and general behaviours in rats and their lactating dams. Male pups were injected in the hind paw with complete Freund’s adjuvant or saline on postnatal day (PN) 1. After weaning, dams were tested for anxiety, sleep recording or hormone profiling (ACTH, corticosterone and prolactin) and brain sampling (pineal melatonin and hippocampus serotonin). At adulthood (PN90), distinct subgroups of neonatal arthritic (AR) and control rats (CR) were also assessed for anxiety and pain thresholds, sleep recording, and blood/brain sampling. Compared to their respective controls at PN12, dams of arthritic rats (DAR) showed a longer latency in expressing pup retrieval and dam–pup interaction. DAR and AR showed a lower pain threshold, anxiety-like behaviour, and sleep fragmentation. Compared to controls, DAR displayed longer sleep latency, reduced paradoxical sleep latency and sleep efficiency, a decrease in prolactin and serotonin levels and increased melatonin levels. This model of unilateral hindpaw inflammation has a wide range of long-term effects in both lactating dams and their adult offspring.

ObjectiveTo evaluate the prevalence of vitamin B12deficiency and factors associated with vitamin B12status in Amazonian children.DesignGenetic risk score (GRS), socio-economic and nutritional status, and morbidity data were the independent variables used in multiple linear regression models to evaluate factors associated with vitamin B12status in a population-based cross-sectional study. GRS was created by summing a number of known risk alleles for low serum vitamin B12.SettingAcrelândia, western Brazilian Amazon.SubjectsChildren (n988) aged ResultsOverall prevalence of vitamin B12deficiency (β=0·017,P=0·030) and animal protein intake(β=0·219,P=0·003) were positively associated with vitamin B12status. GRS (β=−0·114,Pβ=–0·049,P12status was positively associated with wealth index (β=0·012,PZ-score (β=0·024, P=0·033) and serum vitamin A (β=0·089,P<0·001). Age≥60 months(β=–0·118,P<0·001), GRS (β=–0·048, P<0·001), maternal schooling β=–0·083,P<0·001), low intake of animal-derived foods (β=–0·050,P=0·030), serum homocysteine (β=–0·053,P<0·001), serum folate ≥23·6 nmol/l (β=–0·055,P=0·012) and geohelminth infection (β=–0·141,P=0·017) were negatively associated with vitamin B12status.ConclusionsGRS, poverty, low intake of animal-derived foods, geohelminth infection, vitamin A and folate status were important factors associated with vitamin B12status of children in our study.

Rat cisternal (CSF) hypocretin-1 in cerebrospinal fluid was measured after 6 or 96 h of REM sleep deprivation and following 24 h of REM sleep rebound. REM deprivation was found to increase CSF hypocretin-1 collected at zeitgeber time (ZT) 8 but not ZT0. Decreased CSF hypocretin levels were also observed at ZT8 after 24 h of REM sleep rebound. These results suggest that REM sleep deprivation activates and REM sleep rebound inhibits the hypocretin system. Increased hypocretin tone during REM deprivation may be important in mediating some of the effects of REM sleep deprivation such as antidepressant effects, hyperphagia and increased sympathetic activity.

Elevated levels of homocysteine (Hcy) have been associated with major depressive (MD) illness. As human females show a higher predisposition towards depression, this study examined how Hcy levels in rats are affected by sex and estrous cycle in the learned helplessness (LH) model of depression. Male and female rats in either estrus or diestrus were subjected to LH, with intervals of 4 days between the two stress tests and between tests and sacrifice, in order to accommodate the female estrous cycle. No differences were found in LH behavior between males and females at either estrous phase. Control Hcy levels were significantly lower in females than in males (-36%, P

a b s t r a c t The ventrolateral preoptic area (VLPO) has been recognized as one of the key structures responsible for the generation of non-REM (NREM) sleep. The melanin-concentrating hormone (MCH)-containing neurons, which are located in the lateral hypothalamus and incerto-hypothalamic area, project widely throughout the central nervous system and include projections to the VLPO. The MCH has been associ- ated with the central regulation of feeding and energy homeostasis. In addition, recent findings strongly suggest that the MCHergic system promotes sleep. The aim of the present study was to determine if MCH generates sleep by regulating VLPO neuronal activity. To this purpose, we characterized the effect of unilateral and bilateral microinjections of MCH into the VLPO on sleep and wakefulness in the rat. Uni- lateral administration of MCH into the VLPO and adjacent dorsal preoptic area did not modify sleep. On the contrary, bilateral microinjections of MCH (100 ng) into these areas significantly increased light sleep (LS, 39.2 ± 4.8 vs. 21.6 ± 2.5 min, P < 0.05) and total NREM sleep (142.4 ± 23.2 vs. 86.5 ± 10.5 min, P < 0.05) compared to control (saline) microinjections. No effect was observed on REM sleep. We conclude that MCH administration into the VLPO and adjacent dorsal lateral preoptic area promotes the generation of NREM sleep.

Background Evidence suggests that sleep loss is associated with an increased risk of obesity and diabetes; however, animal models have failed to produce weight gain under sleep deprivation (SD). Previous studies have suggested that this discrepancy could be due to more extreme SD conditions in experimental animals, their higher resting metabolic rate than that of humans, and the decreased opportunity for animals to ingest high-calorie foods. Thus, our objective was to determine whether diets with different textures/compositions could modify feeding behavior and affect the metabolic repercussions in SD in rats. Methods Three groups of male rats were used: one was designated as control, one was sleep deprived for 96 h by the platform technique (SD-96h) and one was SD-96h followed by a 24-h recovery (rebound). In the first experiment, the animals were fed chow pellets (CPs); in the second, they received high-fat diet and in the third, they were fed a liquid diet (LD). Results We observed that SD induces energy deficits that were related to changes in feeding behavior and affected by the type of diet consumed. Regardless of the diet consumed, SD consistently increased animals' glucagon levels and decreased their leptin and triacylglycerol levels and liver glycogen stores. However, such changes were mostly avoided in the rats on the liquid diet. SD induces a wide range of metabolic and hormonal changes that are strongly linked to the severity of weight loss. Conclusions The LD, but not the CP or high-fat diets, favored energy intake, consequently lessening the energy deficit induced by SD.