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Background: As a result of social isolation during the COVID-19 pandemic, changes in sleep patterns have been observed in many countries, as well as changes in physical activity and screen time. The objective was to investigate sleep duration and quality during the COVID-19 pandemic and its association with physical activity and screen time., Methods: Cross-sectional study with students from a University in Rio de Janeiro who answered an online questionnaire between August 2020 and March 2021. Physical activity was assessed using IPAQ-SF. Sleep was investigated based on questions about duration and sleep quality change, and screen time through self-reported questions. Multinomial logistic regression was performed to assess the association between physical activity and screen time with sleep duration and quality. Secondary analyses investigated the influence of the isolation time on this association. The confounding factors used were diagnosis of COVID-19, time of isolation, anxiety, depression, skin color, and gender., Results: A total of 771 college students with a mean age of 24.5 years (±8.6) answered the questionnaire. About 75% reported more than 8 h of screen time per day and 49.8% were physically inactive. Regarding sleep, 54.9% had worsening sleep, while 40.6% had inadequate sleep duration during the pandemic. Physical activity was associated with improved sleep quality (Odds ratio (OR) 1.72; confidence interval (95% CI) 1.05-2.97). Also, physically active students who spent more than 14 weeks in social isolation demonstrated improved sleep quality (OR 1.99; 95% CI 1.02-3.78) compared to physically inactive individuals. No association was observed for sleep duration. No association was observed between screen time and sleep quality, or sleep duration., Conclusion: During the COVID-19 pandemic, there was considerable worsening of sleep quality, and physical activity was positively associated with improved sleep quality., (© 2024 Wiley Periodicals LLC.)

Studies on brain anatomy can clarify specific evolutionary and behavioural aspects of wild animals. The rich diversity in a broad range of habitats makes carnivorans especially eligible for studying the relations between the brain form and behaviour, cognitive, sensorial and motor traits. This study compared the brain's contour and total and segmented brain volumetry in three species of neotropical carnivorans. CT images of 17 skulls of three species were acquired: Conepatus chinga (n = 6), Galictis cuja (n = 6) and Lontra longicaudis (n = 5). Three-dimensional endocasts allowed for estimating the brain's total and segmented volumes (olfactory bulb, rostral cerebrum, caudal cerebrum and cerebellum/brain stem). The average volume percentage of the segments was compared interspecifically and intraspecifically between the sexes. The otter has a notably more complex gyrification, typical for semiaquatic carnivorans. Proportionally, the olfactory bulb was significantly larger in hog-nosed skunks, possibly due to a better sense of smell for capturing insects. The proportional volumes of the rostral cerebrum, caudal cerebrum and cerebellum/brain stem segments did not differ between these species. Social behaviour traits and tactile, motor and balance skills were probably not sufficiently distinct to reflect differences in the brain segments analysed in these three species., (© 2023 Wiley-VCH GmbH. Published by John Wiley & Sons Ltd.)

The dual inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) is considered as an important strategy for the treatment of Alzheimer's disease. In this study, we applied the bioguided fractionations of Ocotea daphinifolia ethyl acetate active extract to furnish a fraction with high inhibitory activity for AChE and BuChE (82% and 92%, respectively). High-performance liquid chromatography semipreparative purification of this fraction provided two new natural products: 1-β-D-galactopyranosyl-glycerol-2,3-heptanedionate, (1) whose complete chemical structural elucidation was made with spectrometric analysis (MS, 1D, and 2D NMR) and its minor derivative 1-β-D-gulopyranosyl-glycerol-2,3-heptanedionate; (2) which could be characterized by 2D 1 H- 13 C heteronuclear single-quantum correlation spectra analysis. Investigation of the intermolecular interactions with cholinesterases was carried out by molecular docking studies, and results suggested that both compounds are capable to interact with the catalytic site of both enzymes. Compounds 1 and 2 interact with residues of catalytic domains and the peripheral anionic binding site of AChE and BuChE. The results are comparable to those achieved with rivastigmine and galantamine. Thus, this study provides evidence for consideration of the glycosylglycerol from O. daphnifolia as new valuable dual cholinesterases inhibitor., (© 2022 John Wiley & Sons Ltd.)

Puma yagouaroundi is a wild felid with wide distribution on the American continent. This paper aims to describe the origin and motor distribution of the nerves of the brachial plexus of P. yagouaroundi and compare the findings with the available descriptions for the Carnivora order. Fourteen brachial plexuses of specimens collected dead on highways were dissected (five males and two females). In most cases (57%), the brachial plexus originated from the ventral spinal branches of C5, C6, C7, C8 and T1. The C7 branch was the one that most contributed to the formation of the plexus nerves (57.7%). Among all dissected nerves, 23.6% were unisegmental and 76.4% plurisegmental. The radial nerve was the thickest and innervated the largest number of muscles, while the caudal pectoral nerve showed the most varied formation. Intraspecific polymorphisms occurred in the plexus, although the distribution of the nerves to the muscles had an evident constancy among the individuals. Due to the similarities, locoregional blocking techniques may consider the same anatomical landmarks stipulated for domestic cats. Comparison with the descriptions of other carnivorans allows speculating a polymorphism at the plexus origin, in contrast to the conservative innervation of the muscles in the order Carnivora., (© 2022 Wiley-VCH GmbH.)

Anatomical variation in wild canids is rarely described. Altered shapes, uni- or bilaterally situated, were observed in ventral laminae of C6 and/or in C7 vertebral body of two fox species: Lycalopex gymnocercus and Cerdocyon thous. The specimens were young adults, collected dead on highways in southern Brazil. Deformities were considered anatomical variations because apparently there was no interference in function. The occurrence of such variations in two related species from the same area can suggest an environmental common cause rather than genetic issues. Future studies may deepen the understanding between cause and effect of these vertebral deformities in wild canids., (© 2020 Wiley-VCH GmbH.)

Epidemiological and animal studies have demonstrated a strong association between selenium (Se) supplementation and metabolic disorders, we aimed to evaluate whether maternal Se supplementation was able to change metabolic parameters in rats' offspring. Moreover, as Se is a deiodinase (DIO) cofactor, we decided to investigate how thyroid hormones (THs) would be involved in such metabolic changes. Thereby, two groups (n = 6, ~250 g) of female Wistar rats underwent isotonic saline or sodium selenite (1 mg/kg, p.o.) treatments. Although there were no significant differences in body weight between groups, the Se treatment during pregnancy and lactation increased milk intake and the visceral white adipose tissue (WAT) in offspring. The rats whose mothers were treated with Se also presented an improvement in the glucose tolerance test and in the glucose-stimulated insulin secretion. Regarding the lipid metabolism, the Se group had a reduction of triglycerides in the liver and in WAT. These metabolic changes were accompanied by an increase in serum triiodothyronine (T 3 ) and in DIO 2 expression in brown adipose tissue (BAT). We further demonstrate an increased expression of peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α) and nuclear respiratory factor-1 (NRF-1) mRNA in the liver. In adulthood offspring, Se supplementation programs thyroid function, glucose homeostasis, and feeding behaviour. Taken together, there is no indication that Se programming causes insulin resistance. Moreover, we conjecture that these metabolic responses are induced by increased thyroxine (T 4 ) to T 3 conversion by DIO2 in BAT and mediated by altered transcription factors expression associated with oxidative metabolism control in the liver., (© 2020 John Wiley & Sons Australia, Ltd.)

New Findings: What is the central question of this study? Can Na + depletion mobilize Na + from the skin reservoir in ovariectomized rats? Does oestrogen replacement change the amount and the dynamics of skin Na + storage? Is the reduced salt appetite after Na + depletion in ovariectomized rats with oestrogen replacement related to changes in the skin Na + ? What is the main finding and its importance? This work demonstrated that acute body Na + depletion induced by frusemide mobilized the osmotically inactive skin Na + reservoir to become osmotically active. Oestrogen treatment decreased the induced Na + intake in ovariectomized rats but did not modulate the inactive Na + reservoir in control conditions or its mobilization induced by Na + depletion., Abstract: Oestradiol, which is an important hormone for water and electrolyte balance, also has a role in the inhibition of induced Na + appetite. Sodium can be stored in the skin in osmotically active or inactive forms, and this skin Na + reservoir may be involved in the control of body Na + levels during physiopathological challenges. In this study, we investigated whether the effect of sodium depletion by frusemide can mobilize Na + from the skin reservoir and whether oestradiol replacement changes or mobilizes the Na + reserves in the skin. Ovariectomized Wistar rats were treated with vehicle or oestradiol for 7 days to evaluate the effects of oestrogen on the hydroelectrolyte balance, intake responses and skin Na + and water content in basal conditions. Furthermore, the effects of oestrogen were evaluated after 24 h frusemide-induced whole-body Na + depletion. Oestradiol-replaced rats exhibited reduced water intake without any significant changes in salt intake, Na + excretion or water and Na + skin content in basal conditions. After sodium depletion, both vehicle- and oestradiol-treated rats exhibited an increase in the osmotically active skin Na + , which was associated with a decrease of the inactive skin Na + reservoir. Oestrogen decreased the hypertonic saline intake induced by Na + depletion, but it was not associated with any significant changes in the skin Na + reservoir. Thus, sodium depletion is able to change the inactive-active skin Na + reservoir balance. However, the oestrogenic modulation of sodium appetite after Na + depletion is probably not related to the action of this hormone in the skin Na + reservoir balance., (© 2019 The Authors. Experimental Physiology © 2019 The Physiological Society.)

New Findings: What is the central question of this study? The central goal of this study was to understand the effects of central angiotensin-(1-7) on basal and osmotically stimulated water intake in rats. What is the main finding and its importance? This study demonstrated that central administration of angiotensin-(1-7) did not induce thirst in basal conditions but increased water intake after osmotic stimulation, such as water deprivation and salt loading. These results indicate a new function for this peptide, which, in turn, allows for future research on the mechanisms through which angiotensin-(1-7) influences osmotic thirst. Angiotensin-(1-7) [Ang-(1-7)] is generated by type 2 angiotensin-converting enzyme (ACE2) and binds to the MAS receptor. Although it is well known that Ang-(1-7) functionally antagonizes the effects of the classical renin-angiotensin system in several situations, the role of Ang-(1-7) in hydromineral homeostasis is not clear. The aim of this study was to assess the role of Ang-(1-7) on neuroendocrine responses to hyperosmolality in rats. Male Wistar rats were divided into the following three groups: control; 24 h of water deprivation (WD); and 24 h of salt loading (SL; 1.8% NaCl). Intracerebroventricular (i.c.v.) injections of Ang-(1-7) or vehicle were given to assess water intake and plasma concentration of vasopressin. Additionally, the brains from control and WD groups were collected to evaluate gene expression in the subfornical organ (SFO), paraventricular nucleus (PVN) and supraoptic nucleus (SON). It was found that i.c.v. Ang-(1-7) did not change water and salt intake in control rats; however, Ang-(1-7) increased water intake after WD and SL, with no change in salt intake. Plasma vasopressin was not changed by i.c.v. Ang-(1-7) in control or WD rats. Moreover, WD increased Mas gene expression in the SON and PVN, with no changes in Ace2 mRNA levels. In conclusion, Ang-(1-7) increases thirst after osmotic stimuli, indicating that a previous sensitization to its action is necessary. This finding is consistent with the increased Mas gene expression in the PVN and SON after water deprivation., (© 2017 The Authors. Experimental Physiology © 2017 The Physiological Society.)

Premenopausal women are known to show lower incidence of cardiovascular disease than men. During myocardial infarction (MI), homeostatic responses are activated, including the sympathetic autonomic nervous system and the rennin-angiotensin-aldosterone system, which is related to the fluid and electrolyte balance, both aiming to maintain cardiac output. This study sought to perform a serial evaluation of sexual dimorphism in cardiac autonomic control and fluid and electrolyte balance during the development of MI-induced heart failure in rats. Experimental MI was induced in male (M) and female (F) adult (7-9 weeks of age) Wistar rats. The animals were placed in metabolic cages to assess fluid intake and urine volume 1 and 4 weeks after inducing MI (male myocardial infarction (MMI) and female myocardial infarction (FMI) groups). They subsequently underwent echocardiographic evaluation and spectral analysis of heart rate variability. After completing each protocol, the animals were killed for postmortem evaluation and histology. The MMI group showed earlier and more intense cardiac morphological and functional changes than the FMI group, although the extent of MI did not differ between groups (P > 0.05). The MMI group showed higher sympathetic modulation and sodium and water retention than the FMI group (P < 0.05), which may partly explain both the echocardiographic and pathological findings. Females subjected to infarction seem to show attenuation of sympathetic modulation, more favourable fluid and electrolyte balances, and better preserved cardiac function compared to males subjected to the same infarction model., (© 2016 John Wiley & Sons Australia, Ltd.)

New Findings: What is the central question of this study? The relationship between the thyroid system and sleep deprivation has seldom been assessed in the literature, and mounting evidence exists that sleep disturbances influence human lifestyles. The aim of this study was to investigate the hypothalamic-pituitary-thyroid axis and thyroid hormone metabolism in sleep-deprived and sleep-restricted rats. What is the main finding and its importance? Central hypothyroidism and high thyroxine (T4 ) to 3,5,3'-triiodothyronine (T3 ) activation in brown adipose tissue were observed following sleep deprivation. Sleep-restricted rats exhibited normal thyroid-stimulating hormone and T4 concentrations despite increased circulating T3 . Sleep recovery for 24 h did not normalize the high T3 concentrations, suggesting that high T3 is a powerful counterregulatory mechanism activated following sleep deprivation. Modern life has shortened sleep time, and the consequences of sleep deprivation have been examined in both human subjects and animal models. As the relationship between thyroid function and sleep deprivation has not been fully investigated, the aim of this study was to assess the hypothalamic-pituitary-thyroid axis and thyroid hormone metabolism following paradoxical sleep deprivation (PSD) and sleep restriction (SR) in rats. The effects of a 24 h rebound period were also studied. Male Wistar rats (200-250 g, n = 10 per group) were subjected to sleep deprivation via the modified multiple platform method. Rats were assigned to the following seven groups: control, PSD for 24 or 96 h, 24 or 96 h of sleep deprivation with rebound (PSD24R and PSD96R), SR for 21 days (SR21) and SR21 with rebound (SR21R). Blood samples were collected to determine the 3,5,3'-triiodothyronine (T3 ), thyroxine (T4 ) and thyroid-stimulating hormone concentrations. Brown adipose tissue iodothyronine deiodinase type 2 (D2) activity was also evaluated. Body weight gain was dramatically reduced (by ∼50-100%) in all sleep-deprived and sleep-restricted rats; rebound restored this parameter in only the PSD24R group. The serum TSH and T4 concentrations decreased, whereas T3 increased in both the PSD24 and PSD96 groups compared with control animals (P < 0.05). Only PSD24R and PSD96R normalized T4 and thyroid-stimulating hormone concentrations, respectively, independently of the higher circulating T3 concentrations (∼20-30%) noted in all groups compared with control animals (P < 0.05). Brown adipose tissue D2 activity increased in the PSD 24 and 96 h groups (∼10 times), and PSD24R was more effective than PSD96R at restoring basal brown adipose tissue D2 activity. Our data suggest that thyroid hormone metabolism adapts to sleep deprivation-induced hypothalamic-pituitary-thyroid alterations and increases T4 to T3 activation peripherally, thereby increasing circulating T3 in rats., (© 2014 The Authors. Experimental Physiology © 2014 The Physiological Society.)

Based on the relevance of the renin-angiotensin system and the ongoing controversy regarding the role of the sympathetic nervous system in thyroid hormone-induced cardiac hypertrophy, the aim of the present study was to establish whether the putative difference in the degree of cardiac hypertrophy exhibited by males and females might be related to differences in the sympathetic-vagal balance and/or in the cardiac renin-angiotensin system in mice of different genders. Male and female mice (n = 117) were given 0.1 mg kg(-1) of triiodothyronine or normal saline each day for 10 days consecutively. At the end of that period, study of the heart rate variability, spectral analysis and histopathological examination were performed to assess the sympathetic-vagal balance and the diameter of cardiomyocytes. The cardiac levels of angiotensin I and II were also measured. Treatment with triiodothyronine induced a greater degree of cardiac hypertrophy in male (~73%) than in female mice (~42%). This difference was attributed to greater modulation of the sympathetic nervous system and higher levels of angiotensin I and II in male than in female mice. Our data indicate that thyroid hormone-induced cardiac hypertrophy was more intense in male mice due to the synergic effect of the sympathetic nervous system and the cardiac renin-angiotensin system., (© 2014 The Authors. Experimental Physiology © 2014 The Physiological Society.)

1. The use of angiotensin-converting enzyme (ACE) inhibitors during pregnancy is contraindicated because of their association with increased risks of fetopathy, including central nervous systems malformations. In addition, some reports have shown that renin-angiotensin system components are expressed differently during embryonic development and adulthood in the rat. 2. Because angiotensin II and its derivative peptides have been implicated in anxiety and modulation of nociception, the aim of the present study was to investigate whether inhibiting ACE during prenatal and neonatal periods would alter behavioural plasticity in adult male offspring rats. 3. Female Wistar rats were treated with captopril (2 mg/mL water; approximately 200 mg/kg per day) during pregnancy and lactation. At adulthood, the offspring were subjected to the open field, elevated plus maze, social interaction, forced swimming and tail flick tests. 4. Perinatal captopril treatment significantly increased ambulation (33%; P < 0.05) and decreased resting time (37.5%; P < 0.05) in the open field test. Perinatal captopril treatment did not alter any of the behavioural parameters of the elevated plus maze; however, captopril treatment did cause a significant increase in social interaction (75.3%; P < 0.05). In the forced swimming test, there was an increased latency period (102.9%; P < 0.001) and a decreased immobility period (38.7, P < 0.05) in rats treated with perinatal captopril. In the tail flick test, perinatal captopril treatment significantly reduced the latency time (26.3%; P < 0.01). 5. The data show that ACE inhibition during prenatal and neonatal periods affects behavioural responses in adult offspring rats, suggesting that ACE is required for the development of neural systems that are associated with adult anxiety and nociceptive behavioural responses.

The present work was carried out to investigate the role of angiotensin II type 1 (AT(1)) receptors in nocturnal thirst and sodium appetite induced by classical models of osmotic and sodium depletion challenges in ovariectomized rats chronically treated with oil or oestradiol benzoate (EB, 20 microg per animal, s.c. daily). In both conditions, the animals were given saline or losartan (108 nmol per animal, i.c.v.), a selective AT(1) receptor blocker. Oestrogen therapy significantly reduced the water intake induced by water deprivation, sodium depletion produced by frusemide injected 24 h before, and s.c. acute frusemide plus captopril injection (FUROCAP protocol), with no alteration following s.c. hypertonic saline injection. In contrast, EB therapy decreased the salt intake induced by sodium depletion and FUROCAP protocols, with no alteration following water deprivation and s.c. hypertonic saline injection. Central AT(1) blockade inhibited the dipsogenic response induced by water deprivation, osmotic stimulation, chronic sodium depletion and FUROCAP protocols and inhibited the natriorexigenic response induced by sodium depletion in ovariectomized rats. Oestrogen therapy significantly attenuated the losartan-induced antidipsogenic and antinatriorexigenic actions following sodium depletion and FUROCAP protocols. These results indicate that ovariectomized rats express increased AT(1) receptor signalling related to thirst and sodium appetite responses. Oestrogen therapy and brain AT(1) receptor blockade weakened or markedly decreased the behavioural responses during the nocturnal period, a time at which brain angiotensinergic activity is expected to be more prominent. Finally, we demonstrated through different experimental protocols a clear-cut influence of oestrogenic status on the behavioural AT(1)-induced signalling response.

The present study was carried out to assess the influence of noradrenergic stimulation of the midbrain dorsal (DRN) and median raphe nuclei (MRN) on urinary volume and electrolyte excretion in hydrated rats. Wistar rats were implanted with a guide cannula into the MRN or DRN and then submitted to two intragastric administrations of water in order to attain an increased diuresis. The following treatments were performed. (1) Intra-DRN microinjections of saline (0.2 microl), alpha(1)-adrenergic agonist phenylephrine (PHE, 0.49 and 4.9 nmol in 0.2 microl), alpha(2)-adrenergic antagonist idazoxan (IDZ, 0.42 and 4.2 nmol in 0.2 microl) or the alpha(1)-adrenergic antagonist prazosin (PRZ, 0.24 and 2.4 nmol in 0.2 microl). (2) Intra-MRN microinjections of saline, IDZ (4.2 nmol in 0.2 microl), PHE (4.9 nmol in 0.2 microl) or PRZ (2.4 nmol in 0.2 microl). Urine samples were subsequently collected over 120 min at 20 min intervals for photometric measurement of sodium and potassium. Intra-DRN administration of PHE and IDZ significantly increased the urinary volume, natriuresis and kaliuresis. Intra-DRN microinjection of a higher dose of PRZ reduced the urinary volume and both sodium and potassium excretion. Intra-MRN microinjections of PHE, IDZ or PRZ did not induce any significant effect on urinary volume or electrolyte excretion. These data suggest that the increase of tonic excitatory noradrenergic input conveyed to DRN influences the hydroelectrolyte homeostasis, possibly through 5-HTergic circuitry.

The aim of the present work was to investigate the role of the serotoninergic system in the control of sodium appetite of hypothyroid rats (HTR) by administering drugs that affect the serotoninergic activity, and to compare the same homeostatic behaviour in euthyroid rats (ETR) also given these drugs. Fenfluramine (FEN; 5.0 mg x kg(-1), I.P.), which releases serotonin in the brain, significantly reduced the intake of 1.8 % NaCl in HTR subjected to water and sodium depletion (depleted) or water, sodium and food deprivation (deprived) by 31 and 45 %, respectively, 120 min after FEN injection, compared to HTR that received vehicle alone. Similarly, administration of FEN to ETR reduced 1.8 % NaCl intake in depleted and deprived rats by 64 and 46 %, respectively. The presynaptic serotonin reuptake inhibitor fluoxetine (20.0 mg x kg(-1), I.P.) led to the inhibition of sodium appetite in HTR during the initial 30 min in depleted rats and for up to 60 min post-injection in deprived rats, while sodium appetite inhibition persisted for longer periods in ETR. The 5HT2C receptor agonist mCPP (5.0 mg x kg(-1), I.P.) caused a drastic reduction in sodium appetite in HTR and ETR in depleted and deprived rats, respectively, after 120 min. Prior administration of the 5HT2C receptor antagonist LY53857 (5.0 mg x kg(-1), I.P.) completely blocked the inhibitory action of mCPP on sodium appetite in both HTR and ETR. In summary, our results suggest that the recruitment of serotoninergic neurons involved in the modulation of sodium appetite seems to be decreased in hypothyroidism due to a probable deficiency in the cerebral signalling pathway.

The involvement of angiotensin AT1 receptors in sodium appetite was studied in hypothyroid rats treated with the angiotensin II antagonist losartan. Losartan was administered chronically by the oral route or acutely by the subcutaneous route after water and sodium depletion or water, sodium and food deprivation. Three days after addition of losartan to the food at the dose of 1.0 mg x g(-1), the rats significantly reduced (P < 0.02) their spontaneous intake of 1.8% NaCl. Increasing the dose of losartan to 2.0 and 4.0 mg x g(-1) did not reduce NaCl intake; in contrast, the intensity of the sodium appetite gradually returned to previous levels. The simultaneous administration of captopril, an angiotensin converting enzyme inhibitor, and losartan significantly increased (P < 0.05) NaCl intake and after captopril removal NaCl intake returned to the levels observed with losartan treatment alone. The administration of losartan 4 days after the beginning of captopril treatment significantly reduced (P < 0.0001) NaCl intake. Following acute administration of losartan, water- and sodium-depleted rats significantly reduced their NaCl and water intake (P < 0.001). The administration of losartan also induced a significant reduction in NaCl and water intake in water, NaCl and food-deprived rats (P < 0.0001 and P < 0.001, respectively). The present results show that chronic treatment with oral losartan inhibited spontaneous sodium appetite in hypothyroid rats. Continuation of treatment rendered rats resistant to the blockade of AT1 receptors. Water and sodium depletion and water, NaCl and food deprivation induced sodium appetite, which in the short term depends on cerebral angiotensinergic activity mediated by the activation of AT1 receptors.