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Administration of a high dose of chronic peripheral corticosterone during the postpartum period has been shown to lead to reduced maternal care, but the interference of acute corticosterone, mimicking a situation of acute stress, on maternal behavior has not been well established. Therefore, the aim of our study was to investigate the influence of acute central corticosterone on behavioral and neuroendocrine responses during lactation. On day 7 of lactation, female rats were treated with vehicle (5 μL; i.c.v.) or corticosterone (10 ng/5 μL; i.c.v.) 30 min before the start of the experiment. To evaluate maternal behavior, the pups were returned to the side of their home cages opposite the previous nest, and the resulting behavior of the lactating rats was filmed for the next 30 min. Plasma levels of oxytocin and the amount of milk consumed by the pups were evaluated 15 min after the onset of suckling. In addition, the double-labeled c-Fos/oxytocin neurons in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) and c-Fos immunoreactivity in medial preoptic area (MPOA) neurons were quantified for each lactating rat. Corticosterone decreased maternal care, plasma oxytocin levels, milk consumption by the pups, the activation of oxytocinergic neurons in hypothalamic nuclei, and c-Fos immunoreactivity in MPOA neurons. Our results indicate that changes in the behavioral responses of lactating rats treated with corticosterone may be related to disruption of the neuroendocrine control of oxytocin secretion. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Journal of Physiology & Pharmacology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Lactation is associated with profound behavioral and physiological adaptations in the mother that support reproductive success. These include neuroendocrine adaptation to stress that reduces anxiety-related behavior and emotional responsiveness. However, the way in which endogenous glucocorticoids secreted during immunological challenge influence the neuroendocrine system and behavior of lactating rats is not well understood. To evaluate the effects of glucocorticoids on the neuroendocrine response to suckling, maternal behavior and maternal anxiolysis, lactating female rats were treated with vehicle or metyrapone prior to the administration of a saline solution or a lipopolysaccharide (LPS) solution. LPS treatment reduced oxytocin and prolactin secretion during suckling and affected a variety of maternal behaviors, such as increasing the latency of retrieval a new nest, decreasing the number of pups gathered to the nest, increasing the latency of retrieving the first pup and decreasing the percentage of time spent in the arched-nursing position. In addition, the LPS treatment increased the baseline and avoidance latencies in an elevated T-maze. Pretreatment with metyrapone counteracted effects produced by LPS, including hormonal and behavioral responses in lactating rats. Taken together, our results indicate that stress induced by LPS treatment attenuates the neuroendocrine response to suckling, followed by disruption of maternal behavior and maternal anxiolysis in lactating female rats. These changes may be due to corticosterone release, as evidenced by the reversal of behavioral and neuroendocrine responses after immunological challenge in lactating rats that had been pretreated with metyrapone. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Copyright of Experimental Physiology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Differentiation between organic and conventional coffee has increased due to the growing demand and high consumption of healthy foods that contain compounds with antioxidant potential, which have been associated with the reduction of chronic diseases. We used organic and conventional coffee in powder 4% (w/w) and infusions 5%, 10% and 20% (w/v) incorporated in a commercial diet to test in vivo. The levels of chlorogenic acid, caffeine and trigonelline were determined by high performance liquid chromatography. The body weight, weight gain, food consumption, aberrant foci crypt, mucin depleted foci, stress biomarkers protein carbonyl and malondialdehyde, biochemical parameters and behavior of the rats were compared between the experimental and control groups within a framework of colon carcinogenesis. The organic coffee showed higher levels of chlorogenic acid, caffeine and trigonelline than conventional, however, this difference did not significantly affect behavior. The infusions had an antioxidant effect, reducing the levels of malondialdehyde; however, the biochemical parameters of the serum were not altered, and there was neither induction nor prevention of preneoplasic lesions. [ABSTRACT FROM AUTHOR]

Sepsis-associated encephalopathy, which manifests in severe cognitive and depressive symptoms, is directly linked to neuroinflammation. Our study investigates the efficacy of 25H-NBOMe, a phenethylamine, in alleviating these symptoms, potentially offering an innovative treatment for post-sepsis depression. Wistar rats, weighing between 250–300 g, were subjected to cecal ligation and puncture (CLP) surgery to induce sepsis. Depressive-like behaviors were assessed using the forced swim test (FST) on either day 7 or 14 post-surgery, to establish the presence of depressive symptoms. The impact of 25H-NBOMe treatment was then evaluated, focusing on the head-twitch response (HTR), performance in the FST, and GFAP expression in the prefrontal cortex. Treatment with 25H-NBOMe resulted in significant behavioral changes, demonstrated by decreased immobility and increased swimming times in the FST, along with a rise in the HTR. These outcomes indicate a reduction in depressive-like symptoms post-sepsis and the psychoactive effects of the compound. Furthermore, a notable decrease in GFAP expression in the study highlights the compound's impact on mitigating sepsis-induced astrogliosis. This study demonstrates the effectiveness of 25H-NBOMe, a psychedelic in the phenethylamine class, in treating post-sepsis depression and reducing astrogliosis. However, the psychedelic nature of 25H-NBOMe calls for further investigation into similar compounds with less psychoactive impact, crucial for advancing treatment options for neuropsychiatric symptoms following sepsis. [ABSTRACT FROM AUTHOR]

Abstract: Lactating female rats show a maternal anxiolysis signal, which is part of the behavioral pattern that develops post-partum and seems to be related to hormonal changes during lactation. Assuming that glucocorticoids modulate prolactin and oxytocin secretion, we evaluated the effect of dexamethasone on behavior responses of fear and anxiety in lactating rats. For this study, the non-lactating and lactating rats were submitted to an elevated T-maze and open field tests. In the elevated T-maze, the lactating rats showed a decrease in inhibitory avoidance and an increase in the escape time when compared with the non-lactating group. The lactating rats that had been treated with dexamethasone showed increased initial avoidance latency when compared with lactating rats treated with vehicle. The same result was found in the subsequent repetitions (avoidance 1 and 2). In addition, there was a reduction in one-way escape time for the lactating rats that were treated with dexamethasone. The lactating rats treated with vehicle had increase of number central entries, and consequently, the anti-thigmotactic effect increased relative to non-lactating rats. Thus, lactating rats showed a reduced emotional responsiveness as evaluated by elevated T-maze and open field tests, which characterizes maternal anxiolysis. In addition, it could be concluded that the dexamethasone impairs maternal anxiolysis in lactating female rats. [Copyright &y& Elsevier]

During illnesses caused by infectious diseases, a suite of brain-mediated responses called sickness syndrome occurs, triggering behavioral and physiological changes. This study investigated whether ghrelin modulates sickness syndrome induced by systemic administration of lipopolysaccharide (LPS). Male Wistar rats were pretreated with vehicle or [D-lys3]-GHRP-6, a ghrelin receptor GHS-R1 antagonist (20 nmol, i.c.v), 30 min before injection of LPS (200 μg/kg, i.p.) or sterile saline. We investigated the behavioral effects in male rats after LPS administration by screening for depressive-like behavior, locomotor activity alterations, and corticosterone release. Changes in body temperature were measured using a biotelemetry probe preimplanted in the peritoneal cavity to evaluate the effect of ghrelin on the thermoregulatory response during immunological challenge. Pretreatment with [D-lys3]-GHRP-6 blunted most of the assessed parameters related to sickness syndrome, including social withdrawal, anhedonia, depressive-like behavior, and anorexia, reduced the activation of the HPA axis, but did not alter LPS-induced fever. Our findings suggest that ghrelin centrally mediates the sickness behavior and activation of HPA, as a ghrelin receptor antagonist attenuates social withdrawal, anhedonia, depressive-like behavior, anorexia, and HPA activation in response to LPS. [ABSTRACT FROM AUTHOR]

• Prenatal immune challenge induced sex-specific autistic-like behavior. • MIA results in impaired social interactions in male prepubertal offspring. • Decrease in social play behavior may be associated to hyperactivation of the amygdala. Maternal infection during pregnancy is an environmental risk factor for neurodevelopmental dysfunction, such as autism spectrum disorder (ASD). This study investigated the effect of maternal immune activation (MIA) on the behavior profile of prepubertal offspring and whether MIA alters the neuronal activation pattern of brain areas related to social play behavior. Pregnant Wistar rats received 500 μg/kg of lipopolysaccharide or saline solution on gestational day 16. Their offspring were tested using behavioral tasks to capture some of the core and associated ASD-like symptoms. Neuronal activation, indexed via c-fos expression after social play behavior, was evaluated in several brain areas. MIA had a number of adverse effects on dams and reduced the number of successful births and litter size. MIA induced sex-specific autistic‐like features by a reduction in ultrasonic vocalizations in response to separation from the mother and nest, reduction in discrimination between neutral odors and their nest odor, moderate effect in stereotypies in the hole-board test, impaired risk assessment phenotype, and reduction in social play behavior without changes in locomotor activity only in prepubertal male offspring. A decrease in social play behavior may be associated with a decrease in the number of c-fos-positive cells in the prefrontal cortex and striatum, but hyperactivation of the basolateral and basomedial amygdala. Prenatal immune challenge results in ASD-like symptoms such as impaired risk assessment behavior, communication, and social interactions in male prepubertal offspring. Impaired social play behavior is correlated with neuronal hyperactivation in the amygdala. [ABSTRACT FROM AUTHOR]

Sickness behavior reflects a state of altered physiology and central nervous system function that occurs during systemic infection or inflammation, serving as an adaptive response to illness. This study aims to elucidate the role of hydrogen sulfide (H 2 S) in regulating sickness behavior and neuroinflammatory responses in a rat model of systemic inflammation. Adult male Wistar rats were treated with lipopolysaccharide (LPS) to induce sickness behavior. Intracerebroventricular (i.c.v.) pretreatments included aminooxyacetic acid (AOAA), an inhibitor of H 2 S synthesis, and sodium sulfide (NaHS), an H 2 S donor. Behavioral assays were conducted, along with the assessment of astrocyte activation, as indicated by GFAP expression in the hypothalamus. Pretreatment with NaHS mitigated LPS-induced behavioral changes, including hypophagia, social and exploratory deficits, without affecting peripheral cytokine levels, indicating a central modulatory effect. AOAA, conversely, accentuated certain behavioral responses, suggesting a complex role of endogenous H 2 S in sickness behavior. These findings were reinforced by a lack of effect on plasma interleukin levels but significant reduction in GFAP expression. Our findings support the central role of H 2 S in modulating neuroinflammation and sickness behavior, highlighting the therapeutic potential of targeting H 2 S signaling in neuroinflammatory conditions. • Hydrogen sulfide eases behavioral impact of lipopolysaccharide in rats. • NaHS counters LPS-induced behavioral changes effectively in rodent models. • AOAA enhances LPS-induced hypophagia, pointing to complex H2S roles. • H2S demonstrates significant neuroprotective actions against LPS in CNS. • NaHS icv use shows no change in cytokine levels LPS-induced, indicating central action. [ABSTRACT FROM AUTHOR]

• Neonatal repetitive pain in rats did not change maternal behavior. • Neonatal repetitive pain did not affect basal thresholds to mechanical stimuli. • Male and female offspring had a reduction in mechanical threshold after CFA challenge. • Female animals showed higher formalin-induced hypersensitivity compared to males. Newborn infants are vulnerable to procedural stress and pain exposure on the first weeks of life that represents a critical period for the development of nociceptive, sensory, emotional, and social functions. We evaluated the nociceptive behavior of adult male and female rats that were submitted to nociceptive experience in the neonatal period and the maternal behavior in the postnatal period. The animals were submitted to repetitive needle pricking from the second to the fifteenth postnatal day (PND 2–15). Maternal behavior and litter weight were evaluated during this period. Mechanical sensitivity to pain was assessed in offsprings during the adulthood by exposing them to inflammatory stimuli, including formalin test or the Freund's complete adjuvant (CFA) injection followed by the electronic von Frey test at 0, 3, 6 and 24 h later. Maternal behavior and litter weight were not altered by pinprick stimuli during PND 2–15. Additionally, pinprick stimulation reduced the paw withdrawal threshold in CFA-injected animals compared to control. In the formalin test, there was a difference between the genders. Female rats are statically more sensitive to formalin stimulation and showed an increased licking time in both the first and second phases and increased number of flinches in second phase. Experiencing early life repetitive pain exposure increased inflammatory pain sensitivity in adult offspring rats and female rats are more sensitive to chemical stimulation. Future investigations of the mechanisms involved in this effect may contribute to the improvement of the understanding of inflammatory pain sensitivity differences. [ABSTRACT FROM AUTHOR]

Ring-substituted phenethylamines are believed to induce psychedelic effects primarily by interacting with 5-hydroxytryptamine 2 (5-HT2A) receptors in the brain. We assessed the effect of the psychedelic substances 25H-NBOMe and 25H-NBOH on the depressive-like behavior of male adult rats. Naive Wistar rats were divided into groups to assess the effects of different doses (0.1 mg/kg, 1 mg/kg, and 3 mg/kg) of 25H-NBOMe and 25H-NBOH. The substances were administered intraperitoneally and the hallucinogenic properties were evaluated using the head twitch response test (HTR). Additionally, we assessed their locomotor activity in the open field test (OFT) and depressive-like behavior in the forced swimming test (FST). Our data demonstrated that all doses of synthetic psychedelic substances evaluated exhibited hallucinogenic effects. Interestingly, we observed that both 25H-NBOMe and 25H-NBOH produced a significantly greater motivation to escape in the FST, compared to the control group. Furthermore, we found no significant differences in locomotor activity during the OFT, except for the dose of 3 mg/kg, which induced a reduction in locomotion. This study provides new insights into a potential psychedelic substance, specifically by demonstrating the previously unknown antidepressant properties of a single dose of both 25H-NBOMe and 25H-NBOH. These findings contribute to the ongoing progress of experimental psychiatry toward developing safe and effective clinical practices in the field of psychedelics research. [ABSTRACT FROM AUTHOR]

The involvement of purinergic signaling in several brain functions has been recognized, but the modulation on maternal behavior by the purinergic system is not established, even though there are functional interactions between the purinergic and oxytocinergic systems. Therefore, the aim of our study was to investigate whether central administration of P2 receptor antagonists affected the maternal behavior of lactating rats and c-Fos immunoreactivity in the forebrain. On day 7 of lactation, female rats were treated with vehicle (5 μL; i.c.v.), suramin (9.4–75.0 μg/5 μL; i.c.v.) or PPADS (9.4–75.0 μg/5 μL; i.c.v.) 30 min before the experiment began. The maternal behavior was evaluated during the 30 min following suramin or PPADS administration. In addition, c-Fos-positive nuclei were counted in the medial preoptic area (MPOA) and in the bed nucleus of the stria terminalis (BNST), and neurons that were double-labeled for c-Fos/OT were counted in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus of lactating rats. The results show that P2 receptor antagonists decreased maternal care and decreased neuronal activation in the MPOA and BNST and activation of oxytocinergic neurons in hypothalamic nuclei. Our results indicate that the purinergic system modulates maternal behavior and neuronal activation induced by suckling during lactation. [ABSTRACT FROM AUTHOR]

Thyroid hormones are important for the development of the central nervous system. Since the fetal thyroid gland is not functioning until mid-gestation, transport of maternal thyroid hormones across the placenta is essential during the early phases of gestation. Maternal thyroid deficiency has been associated with a higher incidence of neurodevelopmental disorders in the newborns. The relationship between maternal hypothyroidism and the onset of autism spectrum disorders (ASD) in the offspring, however, is still debated. To address this issue, we used a validated animal model of prenatal hypothyroidism based on the administration of the thyroid peroxidase inhibitor methimazole (MMI, 0.02 g/100 ml in tap water) to rat dams from gestational day 9 up to delivery. The offspring was tested in behavioral tasks during infancy (PNDs 5, 9, 13) and adolescence (PND 35-40) to capture some of the core and associated symptoms of ASD. MMI-exposed pups were able to vocalize as controls when separated from the nest, and showed intact social discrimination abilities in the homing behavior test. At adolescence, the offspring from both sexes did not show an anxious-phenotype in the elevated plus maze and showed intact object recognition. However, MMI-exposed male rats showed increased novelty-directed exploratory behaviors: they solicited their partner to play more and showed more interest for novel rather than familiar objects compared to control rats. Our results show that prenatal MMI-induced hypothyroidism does not cause in the rat offspring behaviors that resemble core and associated ASD symptoms, like deficits in communication and social interaction and anxiety. [ABSTRACT FROM AUTHOR]

Maternal alcohol use during pregnancy adversely affects prenatal and postnatal growth and increases the risk of behavioral deficits. The aim of the present study was to evaluate the effect of prenatal exposure to a moderate dose of alcohol on sexual motivation during adulthood. Rats were prenatally exposed to ethanol by feeding pregnant dams a liquid diet containing 25% ethanol-derived calories on days 6 through 19 of gestation. The controls consisted of pair-fed dams (receiving an isocaloric liquid diet containing 0% ethanol-derived calories) and dams with ad libitum access to a liquid control diet. The sexual motivation of offspring was evaluated during adulthood. The results revealed that the male and female pups of dams treated with alcohol exhibited reduced weight gain, which persisted until adulthood. Both male and female adult animals from dams that were exposed to alcohol showed a reduction in the preference score in the sexual motivation test. Taken together, these results provide evidence of the damaging effects of prenatal alcohol exposure on sexual motivation responses in adulthood. [ABSTRACT FROM AUTHOR]

This study investigated behavioral responses to an immune challenge among animals with fructose-induced metabolic disorders. Adult male Wistar rats were provided either water or a fructose solution (10%) for 5 weeks. Sickness behaviors were assessed 2 h following the injection of either a lipopolysaccharide (LPS) or vehicle. The rats were subjected to an open field test, a social interaction test, a food intake test and a fever evaluation. Cytokine expression was assessed in both adipose tissue and hypothalamus samples. The neural response was assessed in the forebrain immunohistochemistry for c-Fos. Compared with the control group, the fructose diet induced dyslipidemia and significantly higher plasma total cholesterol, HDL-cholesterol, triglyceride, and glucose levels as well as both epididymal and retroperitoneal adiposity. Furthermore, in response to LPS (1 mg/kg), the rats subjected to a fructose diet exhibited exacerbated sickness behaviors and accentuated febrile responses. LPS induced Fos protein expression in several areas of the brains of the control rats; however, higher numbers of Fos-positive cells were observed in the brains of the rats that were fed a fructose diet. Moreover, larger increases in cytokine expression were observed in both the hypothalamus and the adipose tissue of the obese rats compared with the control rats in response to LPS. In this study, fructose diets played an important role in both the induction of metabolic disorders and the modulation of sickness behaviors in response to an immunological challenge, most likely through the induction of cytokines in the hypothalamus. [ABSTRACT FROM AUTHOR]

• LPS-induced sickness behavior was assessed by behavioral tests. • Curcumin decreased LPS-induced plasma levels of cytokines. • Curcumin increased Nrf2 translocation to the cell nucleus. • Curcumin abrogated sickness behavior and fever in rats. Lipopolysaccharide (LPS) is a potent inducer of inflammation, triggering behavioral changes and fever. The present study aimed to evaluate whether pretreatment with curcumin prevents the behavioral changes and fever induced by LPS through the modulation of nuclear factor-erythroid 2 related factor 2 (Nrf2). Male Wistar rats received either vehicle or LPS and after 2 h, the behavioral responses were assessed through open field test (OFT), social interaction test, forced swim test (FST), and food intake assessment. The febrile response was assessed by telemetry after vehicle or LPS injection to evaluate the effect of curcumin on the thermoregulatory response during the immunological challenge. The pretreatment with curcumin at doses of 50 and 100 mg/kg prevented the reduction of distance traveled on OFT, increased the immobility time of FST, impaired social withdrawal, decreased food intake, and induced fever. In addition, at these doses, it was possible to observe a significant decrease in the plasma levels of cytokines and an increase in Nrf2 translocation to the cell nucleus during the immunological challenge. Our data provide further evidence of curcumin's ability to prevent LPS-induced sickness behavior and fever possibly by a mechanism related to the modulation of Nrf2 translocation. [ABSTRACT FROM AUTHOR]

We assessed the influence of maternal overweight on the behavioral neurodevelopment of male and female offspring in prepubertal age by reducing the litter size. To reduce litter size in Wistar rats, the offspring of generation 0 (G0) were culled for 12 pups (6 males and 6 females: normal litter, NL-G1) or 4 pups (2 males and 2 females: small litter, SL-G1). In G1 dams, overweight was characterized, maternal behavior and locomotor activity were assessed. At G2, we quantified the ultrasonic vocalizations in post-natal day 5 (PND5); we evaluated olfactory discrimination in the homing behavior test on PND13; and in PND28–32 (prepubertal age), we performed the following tests: social play behavior, hole board, object recognition, and open field. At the end of the experiments, hippocampus and prefrontal cortex were dissected to quantify the synaptophysin by western blotting. Our data demonstrated that a reduction in litter size was able to induce maternal overweight without altering the parameters related to overweight in the offspring. The SL-G2 offspring showed deficits in early social communication, olfactory discrimination, social play behavior, and the exploration of objects, in addition to increasing repetitive and stereotyped movements. There were also changes in the synaptophysin levels in the hippocampus and prefrontal cortex of the offspring from reduced litter dams. In conclusion, maternal overweight caused by litter reduction impairs behavioral neurodevelopment, inducing autism-like symptoms in the offspring. This study alerts the public about the negative consequences of maternal overweight in the descendants. [ABSTRACT FROM AUTHOR]

• Maternal separation increases an animal's sensitivity to painful chemical stimulation. • Maternal separation reduces the activity of serotonin and norepinephrine neurons. • Serotonin or norepinephrine reuptake inhibitor prevented the increased sensitivity to pain. Animals subjected to early life maternal separation exhibit increased sensitivity to chemical, thermal, and mechanical stimuli during adulthood. However, the mechanism by which maternal separation can alter pain sensitivity in adulthood has not yet been investigated. Thus, we aimed to evaluate the activity of serotonergic and noradrenergic neurons and the effect of serotonin (5-HT) and noradrenaline (NA) reuptake inhibitors in male and female Wistar rats subjected to maternal separation. This study consisted of two experiments: 1) to confirm whether maternal separation increased pain sensitivity (n = 8 per group) and to evaluate the activity of serotonergic neurons in the dorsal raphe nucleus and noradrenergic neurons in locus coeruleus in animals subjected to maternal separation in comparison to controls (n = 6 per group); and 2) to evaluate the effect of fluoxetine (a selective 5-HT reuptake inhibitor) and desipramine (a NA reuptake inhibitor) on sensitivity to chemical stimulation using formalin in animals subjected to maternal separation (n = 8 per group). Our findings indicated that maternal separation increases an animal's sensitivity to painful chemical stimulation and reduces the activity of 5-HT and NA neurons. In addition, acute pretreatment with a 5-HT or NA reuptake inhibitor prevented the increased response to painful stimulation induced by maternal separation. In conclusion, maternal separation increases pain sensitivity by reducing the activity of serotonergic neurons in the dorsal raphe nucleus and noradrenergic neurons in locus coeruleus. This study contributes to possible treatments for pain in individuals exposed to early life stress. [ABSTRACT FROM AUTHOR]